Left atrial remodeling, hypertrophy, and fibrosis in mouse models of heart failure
Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an i...
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| Published in | Cardiovascular pathology Vol. 30; pp. 27 - 37 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
01.09.2017
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| Abstract | Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic, and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction, and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing nonreperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy, and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction associated with atrial dilation, atrial cardiomyocyte hypertrophy, and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function.
•In a mouse model of cardiac pressure overload, left ventricular remodeling is associated with left atrial dilation, hypertrophy, and fibrosis.•Following left ventricular infarction, mice exhibit marked left atrial remodeling and fibrosis.•Obese diabetic mice have atrial dilation, hypertrophy, and mild atrial fibrosis.•Mice with postinfarction heart failure or pressure overload exhibit myofibrillar loss in atrial cardiomyocytes and perturbed localization of connexin-43. |
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| AbstractList | Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic, and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction, and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing nonreperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy, and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction associated with atrial dilation, atrial cardiomyocyte hypertrophy, and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function. Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic, and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction, and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing nonreperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy, and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction associated with atrial dilation, atrial cardiomyocyte hypertrophy, and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function. •In a mouse model of cardiac pressure overload, left ventricular remodeling is associated with left atrial dilation, hypertrophy, and fibrosis.•Following left ventricular infarction, mice exhibit marked left atrial remodeling and fibrosis.•Obese diabetic mice have atrial dilation, hypertrophy, and mild atrial fibrosis.•Mice with postinfarction heart failure or pressure overload exhibit myofibrillar loss in atrial cardiomyocytes and perturbed localization of connexin-43. Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing non-reperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction, associated with atrial dilation, atrial cardiomyocyte hypertrophy and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function. Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic, and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction, and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing nonreperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy, and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction associated with atrial dilation, atrial cardiomyocyte hypertrophy, and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function.Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic, and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction, and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing nonreperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy, and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction associated with atrial dilation, atrial cardiomyocyte hypertrophy, and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function. Abstract Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated. Our study describes the geometric, morphologic and structural changes in experimental mouse models of cardiac pressure overload (induced through transverse aortic constriction), myocardial infarction and diabetes. Morphometric and histological analysis showed that pressure overload was associated with left atrial dilation, increased left atrial mass, loss of myofibrillar content in a subset of atrial cardiomyocytes, atrial cardiomyocyte hypertrophy, and atrial fibrosis. In mice undergoing non-reperfused myocardial infarction protocols, marked left ventricular systolic dysfunction was associated with left atrial enlargement, atrial cardiomyocyte hypertrophy and atrial fibrosis. Both infarcted animals and pressure overloaded mice exhibited attenuation and perturbed localization of atrial connexin-43 immunoreactivity, suggesting gap junctional remodeling. In the absence of injury, obese diabetic db/db mice had diastolic dysfunction, associated with atrial dilation, atrial cardiomyocyte hypertrophy and mild atrial fibrosis. Considering the challenges in assessment of clinically relevant functional endpoints in mouse models of heart disease, study of atrial geometry and morphology may serve as an important new tool for evaluation of ventricular function. |
| Author | Frangogiannis, Nikolaos G. Russo, Ilaria Hanif, Waqas Li, Na Su, Ya Alex, Linda Shinde, Arti V |
| Author_xml | – sequence: 1 givenname: Waqas surname: Hanif fullname: Hanif, Waqas – sequence: 2 givenname: Linda surname: Alex fullname: Alex, Linda – sequence: 3 givenname: Ya surname: Su fullname: Su, Ya – sequence: 4 givenname: Arti V surname: Shinde fullname: Shinde, Arti V – sequence: 5 givenname: Ilaria surname: Russo fullname: Russo, Ilaria – sequence: 6 givenname: Na surname: Li fullname: Li, Na – sequence: 7 givenname: Nikolaos G. surname: Frangogiannis fullname: Frangogiannis, Nikolaos G. email: nikolaos.frangogiannis@einstein.yu.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28759817$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1161/JAHA.115.001925 10.1016/j.jacc.2013.08.1622 10.1093/europace/euw161 10.1371/journal.pone.0125541 10.1093/cvr/cvu176 10.1016/j.jcmg.2016.11.003 10.1016/j.yjmcc.2015.12.011 10.1016/j.carpath.2011.11.007 10.1007/s00018-013-1349-6 10.1161/CIRCRESAHA.113.302593 10.1016/j.ahj.2005.04.031 10.1093/cvr/cvw092 10.1369/0022155413493912 10.1016/j.carpath.2013.12.001 10.1016/j.jacc.2004.03.062 10.1093/cvr/cvw071 10.1016/S0735-1097(97)00184-8 10.1016/j.jacc.2015.03.557 10.1016/j.echo.2008.11.023 10.1002/cphy.c150006 10.1111/j.1600-0560.2007.00943.x 10.1152/ajpheart.00580.2011 10.1007/s00418-008-0541-5 10.1016/j.amjcard.2004.05.060 10.1161/CIRCRESAHA.107.153858 10.1016/j.yjmcc.2015.11.001 10.1172/JCI87491 10.1016/j.ajpath.2015.12.017 10.1016/S0894-7317(05)80356-6 10.1016/j.trsl.2014.05.001 10.1007/BF00788278 10.1016/S0008-6363(02)00273-0 10.1016/j.carpath.2014.03.004 10.1161/CIRCHEARTFAILURE.114.001963 10.1016/S0735-1097(01)01443-7 10.1016/j.yjmcc.2015.11.034 10.1016/j.jdiacomp.2014.07.010 10.1016/j.echo.2009.09.016 10.1016/j.jjcc.2015.04.002 10.1371/journal.pone.0072651 10.1038/ncpcardio1370 10.1161/HYPERTENSIONAHA.111.175323 10.1161/01.CIR.0000066318.21784.43 10.1016/j.jacc.2004.09.054 10.1007/s11010-016-2849-0 10.1073/pnas.88.18.8277 10.1136/hrt.2006.101261 10.1093/cvr/cvx053 |
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| Keywords | Myocardial infarction Heart failure Diabetes Atrial remodeling Fibrosis Hypertrophy heart failure atrial remodeling fibrosis hypertrophy diabetes myocardial infarction |
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| References | Atas, Kepez, Atas, Kanar, Dervisova, Kivrak (bb0195) 2014; 28 Hurrell, Nishimura, Ilstrup, Appleton (bb0170) 1997; 30 De Jong, Van Gelder, Vreeswijk-Baudoin, Cannon, Van Gilst, Maass (bb0105) 2013; 8 Kizer, Bella, Palmieri, Liu, Best, Lee (bb0040) 2006; 151 Rai, Sharma, Agrawal, Agrawal (bb0075) 2017; 424 Takahashi, Sasano, Sugiyama, Kurokawa, Tamura, Soejima (bb0215) 2016; 90 Thomas, Abhayaratna (bb0050) 2017; 10 Emde, Heinen, Godecke, Bottermann (bb0160) 2014; 58 Whittaker, Kloner, Boughner, Pickering (bb0165) 1994; 89 Xia, Dobaczewski, Gonzalez-Quesada, Chen, Biernacka, Li (bb0130) 2011; 58 Ishikawa, Aguero, Oh, Hammoudi, Fish, Leonardson (bb0180) 2015; 4 Christia, Bujak, Gonzalez-Quesada, Chen, Dobaczewski, Reddy (bb0150) 2013; 61 Goudis, Korantzopoulos, Ntalas, Kallergis, Ketikoglou (bb0200) 2015; 66 Corradi, Callegari, Maestri, Benussi, Alfieri (bb0235) 2008; 5 Moller, Hillis, Oh, Seward, Reeder, Wright (bb0010) 2003; 107 Russo, Frangogiannis (bb0225) 2016; 90 Frangogiannis (bb0070) 2015; 5 Kerns, Darst, Olsen, Fenster, Hall, Grevey (bb0155) 2008; 35 Frangogiannis (bb0100) 2017; 127 Kong, Christia, Frangogiannis (bb0080) 2014; 71 Pritchett, Mahoney, Jacobsen, Rodeheffer, Karon, Redfield (bb0005) 2005; 45 Nagueh, Appleton, Gillebert, Marino, Oh, Smiseth (bb0145) 2009; 22 Saxena, Shinde, Haque, Wu, Chen, Su (bb0135) 2015; 89 Beinart, Boyko, Schwammenthal, Kuperstein, Sagie, Hod (bb0015) 2004; 44 Colazzo, Castiglioni, Sironi, Fontana, Nobili, Franzosi (bb0110) 2015; 10 Hirsh, Copeland-Halperin, Halperin (bb0065) 2015; 65 Yang, Shim, Kim, Kim, Rhee, Choi (bb0020) 2009; 22 Cavalera, Wang, Frangogiannis (bb0220) 2014; 164 Poulsen, Dahl, Henriksen, Hey, Hoilund-Carlsen, Beck-Nielsen (bb0035) 2013; 62 Zile, Baicu, Stroud, Van Laer, Arroyo, Mukherjee (bb0190) 2012; 302 Rossi, Cicoira, Bonapace, Golia, Zanolla, Franceschini (bb0030) 2007; 93 Simek, Feldman, Haber, Wu, Jayaweera, Kaul (bb0175) 1995; 8 Sedgwick, Riches, Bageghni, O'Regan, Porter, Turner (bb0230) 2014; 23 Sabharwal, Cemin, Rajan, Hickman, Lahiri, Senior (bb0025) 2004; 94 Rockman, Ross, Harris, Knowlton, Steinhelper, Field (bb0115) 1991; 88 Frunza, Russo, Saxena, Shinde, Humeres, Hanif (bb0125) 2016; 186 Tanaka, Zlochiver, Vikstrom, Yamazaki, Moreno, Klos (bb0055) 2007; 101 Corradi (bb0045) 2014; 23 Kostin, Klein, Szalay, Hein, Bauer, Schaper (bb0245) 2002; 54 Goette, Kalman, Aguinaga, Akar, Cabrera, Chen (bb0185) 2016; 18 Xia, Lee, Li, Corbett, Mendoza, Frangogiannis (bb0120) 2009; 131 Gonzalez-Quesada, Cavalera, Biernacka, Kong, Lee, Saxena (bb0090) 2013; 113 Linz, Hohl, Dhein, Ruf, Reil, Kabiri (bb0210) 2016; 110 Polontchouk, Haefliger, Ebelt, Schaefer, Stuhlmann, Mehlhorn (bb0240) 2001; 38 Shinde, Dobaczewski, de Haan, Saxena, Lee, Xia (bb0095) 2017 Nattel (bb0060) 2016; 110 Saito, Teshima, Fukui, Kondo, Nishio, Nakagawa (bb0205) 2014; 104 Biernacka, Cavalera, Wang, Russo, Shinde, Kong (bb0140) 2015; 8 Kemp, Conte (bb0085) 2012; 21 Shinde (10.1016/j.carpath.2017.06.003_bb0095) 2017 Rockman (10.1016/j.carpath.2017.06.003_bb0115) 1991; 88 Polontchouk (10.1016/j.carpath.2017.06.003_bb0240) 2001; 38 Rai (10.1016/j.carpath.2017.06.003_bb0075) 2017; 424 Yang (10.1016/j.carpath.2017.06.003_bb0020) 2009; 22 Zile (10.1016/j.carpath.2017.06.003_bb0190) 2012; 302 Sabharwal (10.1016/j.carpath.2017.06.003_bb0025) 2004; 94 Frunza (10.1016/j.carpath.2017.06.003_bb0125) 2016; 186 Christia (10.1016/j.carpath.2017.06.003_bb0150) 2013; 61 Cavalera (10.1016/j.carpath.2017.06.003_bb0220) 2014; 164 Kostin (10.1016/j.carpath.2017.06.003_bb0245) 2002; 54 Hirsh (10.1016/j.carpath.2017.06.003_bb0065) 2015; 65 Gonzalez-Quesada (10.1016/j.carpath.2017.06.003_bb0090) 2013; 113 Biernacka (10.1016/j.carpath.2017.06.003_bb0140) 2015; 8 Hurrell (10.1016/j.carpath.2017.06.003_bb0170) 1997; 30 Colazzo (10.1016/j.carpath.2017.06.003_bb0110) 2015; 10 De Jong (10.1016/j.carpath.2017.06.003_bb0105) 2013; 8 Takahashi (10.1016/j.carpath.2017.06.003_bb0215) 2016; 90 Nattel (10.1016/j.carpath.2017.06.003_bb0060) 2016; 110 Simek (10.1016/j.carpath.2017.06.003_bb0175) 1995; 8 Thomas (10.1016/j.carpath.2017.06.003_bb0050) 2017; 10 Beinart (10.1016/j.carpath.2017.06.003_bb0015) 2004; 44 Frangogiannis (10.1016/j.carpath.2017.06.003_bb0100) 2017; 127 Ishikawa (10.1016/j.carpath.2017.06.003_bb0180) 2015; 4 Tanaka (10.1016/j.carpath.2017.06.003_bb0055) 2007; 101 Saxena (10.1016/j.carpath.2017.06.003_bb0135) 2015; 89 Nagueh (10.1016/j.carpath.2017.06.003_bb0145) 2009; 22 Emde (10.1016/j.carpath.2017.06.003_bb0160) 2014; 58 Atas (10.1016/j.carpath.2017.06.003_bb0195) 2014; 28 Corradi (10.1016/j.carpath.2017.06.003_bb0235) 2008; 5 Poulsen (10.1016/j.carpath.2017.06.003_bb0035) 2013; 62 Whittaker (10.1016/j.carpath.2017.06.003_bb0165) 1994; 89 Sedgwick (10.1016/j.carpath.2017.06.003_bb0230) 2014; 23 Moller (10.1016/j.carpath.2017.06.003_bb0010) 2003; 107 Russo (10.1016/j.carpath.2017.06.003_bb0225) 2016; 90 Kemp (10.1016/j.carpath.2017.06.003_bb0085) 2012; 21 Rossi (10.1016/j.carpath.2017.06.003_bb0030) 2007; 93 Linz (10.1016/j.carpath.2017.06.003_bb0210) 2016; 110 Pritchett (10.1016/j.carpath.2017.06.003_bb0005) 2005; 45 Corradi (10.1016/j.carpath.2017.06.003_bb0045) 2014; 23 Saito (10.1016/j.carpath.2017.06.003_bb0205) 2014; 104 Kizer (10.1016/j.carpath.2017.06.003_bb0040) 2006; 151 Frangogiannis (10.1016/j.carpath.2017.06.003_bb0070) 2015; 5 Kong (10.1016/j.carpath.2017.06.003_bb0080) 2014; 71 Xia (10.1016/j.carpath.2017.06.003_bb0120) 2009; 131 Xia (10.1016/j.carpath.2017.06.003_bb0130) 2011; 58 Goette (10.1016/j.carpath.2017.06.003_bb0185) 2016; 18 Goudis (10.1016/j.carpath.2017.06.003_bb0200) 2015; 66 Kerns (10.1016/j.carpath.2017.06.003_bb0155) 2008; 35 24039788 - PLoS One. 2013 Sep 06;8(9):e72651 25928887 - PLoS One. 2015 Apr 30;10(4):e0125541 25994443 - J Am Heart Assoc. 2015 May 20;4(5):null 21947471 - Hypertension. 2011 Nov;58(5):902-11 17704207 - Circ Res. 2007 Oct 12;101(8):839-47 26948424 - Am J Pathol. 2016 May;186(5):1114-27 22227365 - Cardiovasc Pathol. 2012 Sep-Oct;21(5):365-71 28459429 - J Clin Invest. 2017 May 1;127(5):1600-1612 26654778 - J Mol Cell Cardiol. 2016 Jan;90:38-46 27032673 - Cardiovasc Res. 2016 Jun 1;110(3):371-80 25998669 - J Am Coll Cardiol. 2015 May 26;65(20):2239-51 22287584 - Am J Physiol Heart Circ Physiol. 2012 Apr 1;302(7):H1429-37 25985794 - Circ Heart Fail. 2015 Jul;8(4):788-98 27131507 - Cardiovasc Res. 2016 Jun 1;110(3):295-7 28371893 - Cardiovasc Res. 2017 Jul 1;113(8):892-905 24081879 - Circ Res. 2013 Dec 6;113(12):1331-44 19879733 - J Am Soc Echocardiogr. 2009 Dec;22(12 ):1338-43 9247519 - J Am Coll Cardiol. 1997 Aug;30(2):459-67 18544064 - J Cutan Pathol. 2008 Dec;35(12):1093-6 23649149 - Cell Mol Life Sci. 2014 Feb;71(4):549-74 26542797 - J Mol Cell Cardiol. 2015 Dec;89(Pt B):223-31 19030868 - Histochem Cell Biol. 2009 Apr;131(4):471-81 24076532 - J Am Coll Cardiol. 2013 Dec 24;62(25):2416-21 7535519 - Basic Res Cardiol. 1994 Sep-Oct;89(5):397-410 28057220 - JACC Cardiovasc Imaging. 2017 Jan;10 (1):65-77 24880146 - Transl Res. 2014 Oct;164(4):323-35 19187853 - J Am Soc Echocardiogr. 2009 Feb;22(2):107-33 25578975 - Eur J Histochem. 2014 Dec 17;58(4):2448 18852714 - Nat Clin Pract Cardiovasc Med. 2008 Dec;5(12):782-96 1832775 - Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8277-81 17164482 - Heart. 2007 Nov;93(11):1420-5 16442908 - Am Heart J. 2006 Feb;151(2):412-8 26426469 - Compr Physiol. 2015 Sep 20;5(4):1841-75 27402624 - Europace. 2016 Oct;18(10 ):1455-1490 12695291 - Circulation. 2003 May 6;107(17 ):2207-12 15261927 - J Am Coll Cardiol. 2004 Jul 21;44(2):327-34 25130919 - J Diabetes Complications. 2014 Nov-Dec;28(6):858-62 11527649 - J Am Coll Cardiol. 2001 Sep;38(3):883-91 25082849 - Cardiovasc Res. 2014 Oct 1;104(1):5-14 24462196 - Cardiovasc Pathol. 2014 Mar-Apr;23(2):71-84 15629380 - J Am Coll Cardiol. 2005 Jan 4;45(1):87-92 24746387 - Cardiovasc Pathol. 2014 Jul-Aug;23(4):204-10 23714783 - J Histochem Cytochem. 2013 Aug;61(8):555-70 15374781 - Am J Cardiol. 2004 Sep 15;94(6):760-3 25959929 - J Cardiol. 2015 Nov;66(5):361-9 7710749 - J Am Soc Echocardiogr. 1995 Jan-Feb;8(1):37-47 26705059 - J Mol Cell Cardiol. 2016 Jan;90:84-93 12062341 - Cardiovasc Res. 2002 May;54(2):361-79 27766529 - Mol Cell Biochem. 2017 Jan;424(1-2):123-145 |
| References_xml | – volume: 90 start-page: 38 year: 2016 end-page: 46 ident: bb0215 article-title: High-fat diet increases vulnerability to atrial arrhythmia by conduction disturbance via miR-27b publication-title: J Mol Cell Cardiol – volume: 8 start-page: e72651 year: 2013 ident: bb0105 article-title: Atrial remodeling is directly related to end-diastolic left ventricular pressure in a mouse model of ventricular pressure overload publication-title: PLoS One – volume: 113 start-page: 1331 year: 2013 end-page: 1344 ident: bb0090 article-title: Thrombospondin-1 induction in the diabetic myocardium stabilizes the cardiac matrix in addition to promoting vascular rarefaction through angiopoietin-2 upregulation publication-title: Circ Res – volume: 90 start-page: 84 year: 2016 end-page: 93 ident: bb0225 article-title: Diabetes-associated cardiac fibrosis: cellular effectors, molecular mechanisms and therapeutic opportunities publication-title: J Mol Cell Cardiol – volume: 61 start-page: 555 year: 2013 end-page: 570 ident: bb0150 article-title: Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction publication-title: J Histochem Cytochem – volume: 22 start-page: 107 year: 2009 end-page: 133 ident: bb0145 article-title: Recommendations for the evaluation of left ventricular diastolic function by echocardiography publication-title: J Am Soc Echocardiogr – volume: 164 start-page: 323 year: 2014 end-page: 335 ident: bb0220 article-title: Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities publication-title: Transl Res – volume: 66 start-page: 361 year: 2015 end-page: 369 ident: bb0200 article-title: Obesity and atrial fibrillation: a comprehensive review of the pathophysiological mechanisms and links publication-title: J Cardiol – volume: 22 start-page: 1338 year: 2009 end-page: 1343 ident: bb0020 article-title: Left atrial volume index: a predictor of adverse outcome in patients with hypertrophic cardiomyopathy publication-title: J Am Soc Echocardiogr – volume: 54 start-page: 361 year: 2002 end-page: 379 ident: bb0245 article-title: Structural correlate of atrial fibrillation in human patients publication-title: Cardiovasc Res – volume: 110 start-page: 295 year: 2016 end-page: 297 ident: bb0060 article-title: How does fibrosis promote atrial fibrillation persistence: in silico findings, clinical observations, and experimental data publication-title: Cardiovasc Res – volume: 28 start-page: 858 year: 2014 end-page: 862 ident: bb0195 article-title: Effects of diabetes mellitus on left atrial volume and functions in normotensive patients without symptomatic cardiovascular disease publication-title: J Diabetes Complications – volume: 8 start-page: 37 year: 1995 end-page: 47 ident: bb0175 article-title: Relationship between left ventricular wall thickness and left atrial size: comparison with other measures of diastolic function publication-title: J Am Soc Echocardiogr – volume: 23 start-page: 204 year: 2014 end-page: 210 ident: bb0230 article-title: Investigating inherent functional differences between human cardiac fibroblasts cultured from nondiabetic and type 2 diabetic donors publication-title: Cardiovasc Pathol – volume: 127 start-page: 1600 year: 2017 end-page: 1612 ident: bb0100 article-title: The extracellular matrix in myocardial injury, repair, and remodeling publication-title: J Clin Invest – volume: 18 start-page: 1455 year: 2016 end-page: 1490 ident: bb0185 article-title: EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication publication-title: Europace – volume: 101 start-page: 839 year: 2007 end-page: 847 ident: bb0055 article-title: Spatial distribution of fibrosis governs fibrillation wave dynamics in the posterior left atrium during heart failure publication-title: Circ Res – volume: 104 start-page: 5 year: 2014 end-page: 14 ident: bb0205 article-title: Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats publication-title: Cardiovasc Res – volume: 71 start-page: 549 year: 2014 end-page: 574 ident: bb0080 article-title: The pathogenesis of cardiac fibrosis publication-title: Cell Mol Life Sci – volume: 62 start-page: 2416 year: 2013 end-page: 2421 ident: bb0035 article-title: Left atrial volume index: relation to long-term clinical outcome in type 2 diabetes publication-title: J Am Coll Cardiol – volume: 151 start-page: 412 year: 2006 end-page: 418 ident: bb0040 article-title: Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS) publication-title: Am Heart J – volume: 58 start-page: 902 year: 2011 end-page: 911 ident: bb0130 article-title: Endogenous thrombospondin 1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolism publication-title: Hypertension – volume: 94 start-page: 760 year: 2004 end-page: 763 ident: bb0025 article-title: Usefulness of left atrial volume as a predictor of mortality in patients with ischemic cardiomyopathy publication-title: Am J Cardiol – volume: 58 start-page: 2448 year: 2014 ident: bb0160 article-title: Wheat germ agglutinin staining as a suitable method for detection and quantification of fibrosis in cardiac tissue after myocardial infarction publication-title: Eur J Histochem – volume: 10 start-page: 65 year: 2017 end-page: 77 ident: bb0050 article-title: Left atrial reverse remodeling: mechanisms, evaluation, and clinical significance publication-title: JACC Cardiovasc Imaging – volume: 4 year: 2015 ident: bb0180 article-title: Increased stiffness is the major early abnormality in a pig model of severe aortic stenosis and predisposes to congestive heart failure in the absence of systolic dysfunction publication-title: J Am Heart Assoc – volume: 30 start-page: 459 year: 1997 end-page: 467 ident: bb0170 article-title: Utility of preload alteration in assessment of left ventricular filling pressure by Doppler echocardiography: a simultaneous catheterization and Doppler echocardiographic study publication-title: J Am Coll Cardiol – volume: 45 start-page: 87 year: 2005 end-page: 92 ident: bb0005 article-title: Diastolic dysfunction and left atrial volume: a population-based study publication-title: J Am Coll Cardiol – volume: 424 start-page: 123 year: 2017 end-page: 145 ident: bb0075 article-title: Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research publication-title: Mol Cell Biochem – volume: 5 start-page: 1841 year: 2015 end-page: 1875 ident: bb0070 article-title: Pathophysiology of myocardial infarction publication-title: Compr Physiol – volume: 107 start-page: 2207 year: 2003 end-page: 2212 ident: bb0010 article-title: Left atrial volume: a powerful predictor of survival after acute myocardial infarction publication-title: Circulation – volume: 89 start-page: 223 year: 2015 end-page: 231 ident: bb0135 article-title: The role of interleukin receptor associated kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction publication-title: J Mol Cell Cardiol – volume: 8 start-page: 788 year: 2015 end-page: 798 ident: bb0140 article-title: Smad3 signaling promotes fibrosis while preserving cardiac and aortic geometry in obese diabetic mice publication-title: Circ Heart Fail – volume: 44 start-page: 327 year: 2004 end-page: 334 ident: bb0015 article-title: Long-term prognostic significance of left atrial volume in acute myocardial infarction publication-title: J Am Coll Cardiol – volume: 35 start-page: 1093 year: 2008 end-page: 1096 ident: bb0155 article-title: Shrinkage of cutaneous specimens: formalin or other factors involved? publication-title: J Cutan Pathol – volume: 10 start-page: e0125541 year: 2015 ident: bb0110 article-title: Murine left atrium and left atrial appendage structure and function: echocardiographic and morphologic evaluation publication-title: PLoS One – volume: 23 start-page: 71 year: 2014 end-page: 84 ident: bb0045 article-title: Atrial fibrillation from the pathologist's perspective publication-title: Cardiovasc Pathol – volume: 186 start-page: 1114 year: 2016 end-page: 1127 ident: bb0125 article-title: Myocardial galectin-3 expression is associated with remodeling of the pressure-overloaded heart and may delay the hypertrophic response without affecting survival, dysfunction, and cardiac fibrosis publication-title: Am J Pathol – year: 2017 ident: bb0095 article-title: Tissue transglutaminase induction in the pressure-overloaded myocardium regulates matrix remodeling publication-title: Cardiovasc Res – volume: 65 start-page: 2239 year: 2015 end-page: 2251 ident: bb0065 article-title: Fibrotic atrial cardiomyopathy, atrial fibrillation, and thromboembolism: mechanistic links and clinical inferences publication-title: J Am Coll Cardiol – volume: 88 start-page: 8277 year: 1991 end-page: 8281 ident: bb0115 article-title: Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy publication-title: Proc Natl Acad Sci U S A – volume: 131 start-page: 471 year: 2009 end-page: 481 ident: bb0120 article-title: Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload publication-title: Histochem Cell Biol – volume: 110 start-page: 371 year: 2016 end-page: 380 ident: bb0210 article-title: Cathepsin a mediates susceptibility to atrial tachyarrhythmia and impairment of atrial emptying function in Zucker diabetic fatty rats publication-title: Cardiovasc Res – volume: 5 start-page: 782 year: 2008 end-page: 796 ident: bb0235 article-title: Structural remodeling in atrial fibrillation publication-title: Nat Clin Pract Cardiovasc Med – volume: 38 start-page: 883 year: 2001 end-page: 891 ident: bb0240 article-title: Effects of chronic atrial fibrillation on gap junction distribution in human and rat atria publication-title: J Am Coll Cardiol – volume: 89 start-page: 397 year: 1994 end-page: 410 ident: bb0165 article-title: Quantitative assessment of myocardial collagen with picrosirius red staining and circularly polarized light publication-title: Basic Res Cardiol – volume: 302 start-page: H1429 year: 2012 end-page: H1437 ident: bb0190 article-title: Pressure overload-dependent membrane type 1-matrix metalloproteinase induction: relationship to LV remodeling and fibrosis publication-title: Am J Physiol Heart Circ Physiol – volume: 93 start-page: 1420 year: 2007 end-page: 1425 ident: bb0030 article-title: Left atrial volume provides independent and incremental information compared with exercise tolerance parameters in patients with heart failure and left ventricular systolic dysfunction publication-title: Heart – volume: 21 start-page: 365 year: 2012 end-page: 371 ident: bb0085 article-title: The pathophysiology of heart failure publication-title: Cardiovasc Pathol – volume: 4 issue: 5 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0180 article-title: Increased stiffness is the major early abnormality in a pig model of severe aortic stenosis and predisposes to congestive heart failure in the absence of systolic dysfunction publication-title: J Am Heart Assoc doi: 10.1161/JAHA.115.001925 – volume: 62 start-page: 2416 issue: 25 year: 2013 ident: 10.1016/j.carpath.2017.06.003_bb0035 article-title: Left atrial volume index: relation to long-term clinical outcome in type 2 diabetes publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2013.08.1622 – volume: 18 start-page: 1455 issue: 10 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0185 article-title: EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication publication-title: Europace doi: 10.1093/europace/euw161 – volume: 10 start-page: e0125541 issue: 4 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0110 article-title: Murine left atrium and left atrial appendage structure and function: echocardiographic and morphologic evaluation publication-title: PLoS One doi: 10.1371/journal.pone.0125541 – volume: 104 start-page: 5 issue: 1 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0205 article-title: Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats publication-title: Cardiovasc Res doi: 10.1093/cvr/cvu176 – volume: 10 start-page: 65 issue: 1 year: 2017 ident: 10.1016/j.carpath.2017.06.003_bb0050 article-title: Left atrial reverse remodeling: mechanisms, evaluation, and clinical significance publication-title: JACC Cardiovasc Imaging doi: 10.1016/j.jcmg.2016.11.003 – volume: 90 start-page: 84 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0225 article-title: Diabetes-associated cardiac fibrosis: cellular effectors, molecular mechanisms and therapeutic opportunities publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2015.12.011 – volume: 21 start-page: 365 issue: 5 year: 2012 ident: 10.1016/j.carpath.2017.06.003_bb0085 article-title: The pathophysiology of heart failure publication-title: Cardiovasc Pathol doi: 10.1016/j.carpath.2011.11.007 – volume: 71 start-page: 549 issue: 4 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0080 article-title: The pathogenesis of cardiac fibrosis publication-title: Cell Mol Life Sci doi: 10.1007/s00018-013-1349-6 – volume: 113 start-page: 1331 issue: 12 year: 2013 ident: 10.1016/j.carpath.2017.06.003_bb0090 article-title: Thrombospondin-1 induction in the diabetic myocardium stabilizes the cardiac matrix in addition to promoting vascular rarefaction through angiopoietin-2 upregulation publication-title: Circ Res doi: 10.1161/CIRCRESAHA.113.302593 – volume: 151 start-page: 412 issue: 2 year: 2006 ident: 10.1016/j.carpath.2017.06.003_bb0040 article-title: Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS) publication-title: Am Heart J doi: 10.1016/j.ahj.2005.04.031 – volume: 110 start-page: 295 issue: 3 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0060 article-title: How does fibrosis promote atrial fibrillation persistence: in silico findings, clinical observations, and experimental data publication-title: Cardiovasc Res doi: 10.1093/cvr/cvw092 – volume: 61 start-page: 555 issue: 8 year: 2013 ident: 10.1016/j.carpath.2017.06.003_bb0150 article-title: Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction publication-title: J Histochem Cytochem doi: 10.1369/0022155413493912 – volume: 23 start-page: 71 issue: 2 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0045 article-title: Atrial fibrillation from the pathologist's perspective publication-title: Cardiovasc Pathol doi: 10.1016/j.carpath.2013.12.001 – volume: 44 start-page: 327 issue: 2 year: 2004 ident: 10.1016/j.carpath.2017.06.003_bb0015 article-title: Long-term prognostic significance of left atrial volume in acute myocardial infarction publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2004.03.062 – volume: 110 start-page: 371 issue: 3 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0210 article-title: Cathepsin a mediates susceptibility to atrial tachyarrhythmia and impairment of atrial emptying function in Zucker diabetic fatty rats publication-title: Cardiovasc Res doi: 10.1093/cvr/cvw071 – volume: 30 start-page: 459 issue: 2 year: 1997 ident: 10.1016/j.carpath.2017.06.003_bb0170 article-title: Utility of preload alteration in assessment of left ventricular filling pressure by Doppler echocardiography: a simultaneous catheterization and Doppler echocardiographic study publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(97)00184-8 – volume: 65 start-page: 2239 issue: 20 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0065 article-title: Fibrotic atrial cardiomyopathy, atrial fibrillation, and thromboembolism: mechanistic links and clinical inferences publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2015.03.557 – volume: 22 start-page: 107 issue: 2 year: 2009 ident: 10.1016/j.carpath.2017.06.003_bb0145 article-title: Recommendations for the evaluation of left ventricular diastolic function by echocardiography publication-title: J Am Soc Echocardiogr doi: 10.1016/j.echo.2008.11.023 – volume: 5 start-page: 1841 issue: 4 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0070 article-title: Pathophysiology of myocardial infarction publication-title: Compr Physiol doi: 10.1002/cphy.c150006 – volume: 35 start-page: 1093 issue: 12 year: 2008 ident: 10.1016/j.carpath.2017.06.003_bb0155 article-title: Shrinkage of cutaneous specimens: formalin or other factors involved? publication-title: J Cutan Pathol doi: 10.1111/j.1600-0560.2007.00943.x – volume: 58 start-page: 2448 issue: 4 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0160 article-title: Wheat germ agglutinin staining as a suitable method for detection and quantification of fibrosis in cardiac tissue after myocardial infarction publication-title: Eur J Histochem – volume: 302 start-page: H1429 issue: 7 year: 2012 ident: 10.1016/j.carpath.2017.06.003_bb0190 article-title: Pressure overload-dependent membrane type 1-matrix metalloproteinase induction: relationship to LV remodeling and fibrosis publication-title: Am J Physiol Heart Circ Physiol doi: 10.1152/ajpheart.00580.2011 – volume: 131 start-page: 471 issue: 4 year: 2009 ident: 10.1016/j.carpath.2017.06.003_bb0120 article-title: Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload publication-title: Histochem Cell Biol doi: 10.1007/s00418-008-0541-5 – volume: 94 start-page: 760 issue: 6 year: 2004 ident: 10.1016/j.carpath.2017.06.003_bb0025 article-title: Usefulness of left atrial volume as a predictor of mortality in patients with ischemic cardiomyopathy publication-title: Am J Cardiol doi: 10.1016/j.amjcard.2004.05.060 – volume: 101 start-page: 839 issue: 8 year: 2007 ident: 10.1016/j.carpath.2017.06.003_bb0055 article-title: Spatial distribution of fibrosis governs fibrillation wave dynamics in the posterior left atrium during heart failure publication-title: Circ Res doi: 10.1161/CIRCRESAHA.107.153858 – volume: 89 start-page: 223 issue: Pt B year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0135 article-title: The role of interleukin receptor associated kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2015.11.001 – volume: 127 start-page: 1600 issue: 5 year: 2017 ident: 10.1016/j.carpath.2017.06.003_bb0100 article-title: The extracellular matrix in myocardial injury, repair, and remodeling publication-title: J Clin Invest doi: 10.1172/JCI87491 – volume: 186 start-page: 1114 issue: 5 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0125 article-title: Myocardial galectin-3 expression is associated with remodeling of the pressure-overloaded heart and may delay the hypertrophic response without affecting survival, dysfunction, and cardiac fibrosis publication-title: Am J Pathol doi: 10.1016/j.ajpath.2015.12.017 – volume: 8 start-page: 37 issue: 1 year: 1995 ident: 10.1016/j.carpath.2017.06.003_bb0175 article-title: Relationship between left ventricular wall thickness and left atrial size: comparison with other measures of diastolic function publication-title: J Am Soc Echocardiogr doi: 10.1016/S0894-7317(05)80356-6 – volume: 164 start-page: 323 issue: 4 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0220 article-title: Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities publication-title: Transl Res doi: 10.1016/j.trsl.2014.05.001 – volume: 89 start-page: 397 issue: 5 year: 1994 ident: 10.1016/j.carpath.2017.06.003_bb0165 article-title: Quantitative assessment of myocardial collagen with picrosirius red staining and circularly polarized light publication-title: Basic Res Cardiol doi: 10.1007/BF00788278 – volume: 54 start-page: 361 issue: 2 year: 2002 ident: 10.1016/j.carpath.2017.06.003_bb0245 article-title: Structural correlate of atrial fibrillation in human patients publication-title: Cardiovasc Res doi: 10.1016/S0008-6363(02)00273-0 – volume: 23 start-page: 204 issue: 4 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0230 article-title: Investigating inherent functional differences between human cardiac fibroblasts cultured from nondiabetic and type 2 diabetic donors publication-title: Cardiovasc Pathol doi: 10.1016/j.carpath.2014.03.004 – volume: 8 start-page: 788 issue: 4 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0140 article-title: Smad3 signaling promotes fibrosis while preserving cardiac and aortic geometry in obese diabetic mice publication-title: Circ Heart Fail doi: 10.1161/CIRCHEARTFAILURE.114.001963 – volume: 38 start-page: 883 issue: 3 year: 2001 ident: 10.1016/j.carpath.2017.06.003_bb0240 article-title: Effects of chronic atrial fibrillation on gap junction distribution in human and rat atria publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(01)01443-7 – volume: 90 start-page: 38 year: 2016 ident: 10.1016/j.carpath.2017.06.003_bb0215 article-title: High-fat diet increases vulnerability to atrial arrhythmia by conduction disturbance via miR-27b publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2015.11.034 – volume: 28 start-page: 858 issue: 6 year: 2014 ident: 10.1016/j.carpath.2017.06.003_bb0195 article-title: Effects of diabetes mellitus on left atrial volume and functions in normotensive patients without symptomatic cardiovascular disease publication-title: J Diabetes Complications doi: 10.1016/j.jdiacomp.2014.07.010 – volume: 22 start-page: 1338 issue: 12 year: 2009 ident: 10.1016/j.carpath.2017.06.003_bb0020 article-title: Left atrial volume index: a predictor of adverse outcome in patients with hypertrophic cardiomyopathy publication-title: J Am Soc Echocardiogr doi: 10.1016/j.echo.2009.09.016 – volume: 66 start-page: 361 issue: 5 year: 2015 ident: 10.1016/j.carpath.2017.06.003_bb0200 article-title: Obesity and atrial fibrillation: a comprehensive review of the pathophysiological mechanisms and links publication-title: J Cardiol doi: 10.1016/j.jjcc.2015.04.002 – volume: 8 start-page: e72651 issue: 9 year: 2013 ident: 10.1016/j.carpath.2017.06.003_bb0105 article-title: Atrial remodeling is directly related to end-diastolic left ventricular pressure in a mouse model of ventricular pressure overload publication-title: PLoS One doi: 10.1371/journal.pone.0072651 – volume: 5 start-page: 782 issue: 12 year: 2008 ident: 10.1016/j.carpath.2017.06.003_bb0235 article-title: Structural remodeling in atrial fibrillation publication-title: Nat Clin Pract Cardiovasc Med doi: 10.1038/ncpcardio1370 – volume: 58 start-page: 902 issue: 5 year: 2011 ident: 10.1016/j.carpath.2017.06.003_bb0130 article-title: Endogenous thrombospondin 1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolism publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.111.175323 – volume: 107 start-page: 2207 issue: 17 year: 2003 ident: 10.1016/j.carpath.2017.06.003_bb0010 article-title: Left atrial volume: a powerful predictor of survival after acute myocardial infarction publication-title: Circulation doi: 10.1161/01.CIR.0000066318.21784.43 – volume: 45 start-page: 87 issue: 1 year: 2005 ident: 10.1016/j.carpath.2017.06.003_bb0005 article-title: Diastolic dysfunction and left atrial volume: a population-based study publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2004.09.054 – volume: 424 start-page: 123 issue: 1–2 year: 2017 ident: 10.1016/j.carpath.2017.06.003_bb0075 article-title: Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research publication-title: Mol Cell Biochem doi: 10.1007/s11010-016-2849-0 – volume: 88 start-page: 8277 issue: 18 year: 1991 ident: 10.1016/j.carpath.2017.06.003_bb0115 article-title: Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.88.18.8277 – volume: 93 start-page: 1420 issue: 11 year: 2007 ident: 10.1016/j.carpath.2017.06.003_bb0030 article-title: Left atrial volume provides independent and incremental information compared with exercise tolerance parameters in patients with heart failure and left ventricular systolic dysfunction publication-title: Heart doi: 10.1136/hrt.2006.101261 – year: 2017 ident: 10.1016/j.carpath.2017.06.003_bb0095 article-title: Tissue transglutaminase induction in the pressure-overloaded myocardium regulates matrix remodeling publication-title: Cardiovasc Res doi: 10.1093/cvr/cvx053 – reference: 27032673 - Cardiovasc Res. 2016 Jun 1;110(3):371-80 – reference: 27131507 - Cardiovasc Res. 2016 Jun 1;110(3):295-7 – reference: 27402624 - Europace. 2016 Oct;18(10 ):1455-1490 – reference: 24039788 - PLoS One. 2013 Sep 06;8(9):e72651 – reference: 9247519 - J Am Coll Cardiol. 1997 Aug;30(2):459-67 – reference: 16442908 - Am Heart J. 2006 Feb;151(2):412-8 – reference: 25959929 - J Cardiol. 2015 Nov;66(5):361-9 – reference: 12695291 - Circulation. 2003 May 6;107(17 ):2207-12 – reference: 25578975 - Eur J Histochem. 2014 Dec 17;58(4):2448 – reference: 17704207 - Circ Res. 2007 Oct 12;101(8):839-47 – reference: 25082849 - Cardiovasc Res. 2014 Oct 1;104(1):5-14 – reference: 1832775 - Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8277-81 – reference: 18852714 - Nat Clin Pract Cardiovasc Med. 2008 Dec;5(12):782-96 – reference: 24462196 - Cardiovasc Pathol. 2014 Mar-Apr;23(2):71-84 – reference: 23714783 - J Histochem Cytochem. 2013 Aug;61(8):555-70 – reference: 28057220 - JACC Cardiovasc Imaging. 2017 Jan;10 (1):65-77 – reference: 7710749 - J Am Soc Echocardiogr. 1995 Jan-Feb;8(1):37-47 – reference: 21947471 - Hypertension. 2011 Nov;58(5):902-11 – reference: 26426469 - Compr Physiol. 2015 Sep 20;5(4):1841-75 – reference: 25994443 - J Am Heart Assoc. 2015 May 20;4(5):null – reference: 25985794 - Circ Heart Fail. 2015 Jul;8(4):788-98 – reference: 15261927 - J Am Coll Cardiol. 2004 Jul 21;44(2):327-34 – reference: 19879733 - J Am Soc Echocardiogr. 2009 Dec;22(12 ):1338-43 – reference: 25130919 - J Diabetes Complications. 2014 Nov-Dec;28(6):858-62 – reference: 25928887 - PLoS One. 2015 Apr 30;10(4):e0125541 – reference: 25998669 - J Am Coll Cardiol. 2015 May 26;65(20):2239-51 – reference: 26654778 - J Mol Cell Cardiol. 2016 Jan;90:38-46 – reference: 19187853 - J Am Soc Echocardiogr. 2009 Feb;22(2):107-33 – reference: 27766529 - Mol Cell Biochem. 2017 Jan;424(1-2):123-145 – reference: 12062341 - Cardiovasc Res. 2002 May;54(2):361-79 – reference: 24081879 - Circ Res. 2013 Dec 6;113(12):1331-44 – reference: 22287584 - Am J Physiol Heart Circ Physiol. 2012 Apr 1;302(7):H1429-37 – reference: 7535519 - Basic Res Cardiol. 1994 Sep-Oct;89(5):397-410 – reference: 11527649 - J Am Coll Cardiol. 2001 Sep;38(3):883-91 – reference: 23649149 - Cell Mol Life Sci. 2014 Feb;71(4):549-74 – reference: 26542797 - J Mol Cell Cardiol. 2015 Dec;89(Pt B):223-31 – reference: 22227365 - Cardiovasc Pathol. 2012 Sep-Oct;21(5):365-71 – reference: 19030868 - Histochem Cell Biol. 2009 Apr;131(4):471-81 – reference: 15374781 - Am J Cardiol. 2004 Sep 15;94(6):760-3 – reference: 24880146 - Transl Res. 2014 Oct;164(4):323-35 – reference: 24076532 - J Am Coll Cardiol. 2013 Dec 24;62(25):2416-21 – reference: 26948424 - Am J Pathol. 2016 May;186(5):1114-27 – reference: 28459429 - J Clin Invest. 2017 May 1;127(5):1600-1612 – reference: 17164482 - Heart. 2007 Nov;93(11):1420-5 – reference: 18544064 - J Cutan Pathol. 2008 Dec;35(12):1093-6 – reference: 26705059 - J Mol Cell Cardiol. 2016 Jan;90:84-93 – reference: 28371893 - Cardiovasc Res. 2017 Jul 1;113(8):892-905 – reference: 15629380 - J Am Coll Cardiol. 2005 Jan 4;45(1):87-92 – reference: 24746387 - Cardiovasc Pathol. 2014 Jul-Aug;23(4):204-10 |
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| Snippet | Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful... Abstract Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful... Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful... |
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| SubjectTerms | Animals Atrial remodeling Atrial Remodeling - physiology Cardiomegaly - etiology Cardiomegaly - pathology Cardiomegaly - physiopathology Connexin 43 - metabolism Diabetes Diabetic Cardiomyopathies - pathology Diabetic Cardiomyopathies - physiopathology Disease Models, Animal Female Fibrosis Heart failure Heart Failure - etiology Heart Failure - pathology Heart Failure - physiopathology Humans Hypertrophy Male Mice Mice, Inbred C57BL Myocardial infarction Myocardial Infarction - pathology Myocardial Infarction - physiopathology Obesity - pathology Obesity - physiopathology Pathology Tachycardia - pathology Tachycardia - physiopathology Ventricular Dysfunction, Left - pathology Ventricular Dysfunction, Left - physiopathology |
| Title | Left atrial remodeling, hypertrophy, and fibrosis in mouse models of heart failure |
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