Macrophage polarization in atherosclerosis
•Effects of macrophages on atherosclerosis are related to macrophage polarization.•Different macrophage phenotypes have different effects on the plaque progress.•Macrophage polarization is the potential targets for treating atherosclerosis. Atherosclerosis is a chronic inflammatory response that inc...
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Published in | Clinica chimica acta Vol. 501; pp. 142 - 146 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.02.2020
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Subjects | |
Online Access | Get full text |
ISSN | 0009-8981 1873-3492 1873-3492 |
DOI | 10.1016/j.cca.2019.10.034 |
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Abstract | •Effects of macrophages on atherosclerosis are related to macrophage polarization.•Different macrophage phenotypes have different effects on the plaque progress.•Macrophage polarization is the potential targets for treating atherosclerosis.
Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization. |
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AbstractList | Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization.Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization. Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization. •Effects of macrophages on atherosclerosis are related to macrophage polarization.•Different macrophage phenotypes have different effects on the plaque progress.•Macrophage polarization is the potential targets for treating atherosclerosis. Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization. |
Author | Jiang, Zhi-Sheng Hao, Ya-Meng Ren, Zhong Tang, Zhi-Han Zhang, Ji-Feng Qu, Shun-Lin Yuan, Hou-Qin Wei, Dang-Heng Yang, Sai Liu, Lu-Shan |
Author_xml | – sequence: 1 givenname: Sai surname: Yang fullname: Yang, Sai organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 2 givenname: Hou-Qin surname: Yuan fullname: Yuan, Hou-Qin organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 3 givenname: Ya-Meng surname: Hao fullname: Hao, Ya-Meng organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 4 givenname: Zhong surname: Ren fullname: Ren, Zhong organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 5 givenname: Shun-Lin surname: Qu fullname: Qu, Shun-Lin organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 6 givenname: Lu-Shan surname: Liu fullname: Liu, Lu-Shan organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 7 givenname: Dang-Heng surname: Wei fullname: Wei, Dang-Heng organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 8 givenname: Zhi-Han surname: Tang fullname: Tang, Zhi-Han organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China – sequence: 9 givenname: Ji-Feng surname: Zhang fullname: Zhang, Ji-Feng organization: Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, 2800 Plymouth Rd, NCRC Bldg26-357S, Ann Arbor, MI 48109, USA – sequence: 10 givenname: Zhi-Sheng surname: Jiang fullname: Jiang, Zhi-Sheng email: zsjiang2005@163.com organization: Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, University of South China, Hengyang City, Hunan Province, 421001, PR China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31730809$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1161/ATVBAHA.115.306132 10.3389/fphar.2018.00464 10.1089/ars.2015.6577 10.1159/000430126 10.5551/jat.RV17020 10.1016/j.ijcard.2015.03.151 10.1161/ATVBAHA.115.305438 10.1016/j.intimp.2017.11.037 10.1038/ncomms7676 10.2353/ajpath.2009.080431 10.1186/s12933-017-0626-3 10.1016/j.jacc.2011.10.852 10.1161/CIRCRESAHA.109.215715 10.1161/ATVBAHA.118.311185 10.1038/srep35234 10.1161/CIRCRESAHA.117.312513 10.1038/74680 10.1089/hum.2018.084 10.1080/10717544.2018.1477860 10.1016/j.pharmthera.2018.02.003 10.1152/ajpcell.00370.2015 10.1016/j.ijcard.2015.07.044 10.1177/1753425914526461 10.1155/2015/909572 10.1161/ATVBAHA.113.300986 10.3390/md15110358 10.1016/j.immuni.2014.06.008 10.3389/fimmu.2018.00878 10.1161/hh2201.099415 10.1111/jcmm.13329 10.1172/JCI75005 10.1161/ATVBAHA.116.308461 10.1016/j.atherosclerosis.2012.09.013 10.1016/j.celrep.2016.09.008 10.4049/jimmunol.0901368 10.1161/CIRCRESAHA.116.310262 10.1161/CIRCRESAHA.111.247577 10.1161/CIRCRESAHA.110.233775 |
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Keywords | Macrophage polarization Phenotype Atherosclerosis |
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References | Zhou, Zhang, Wang, Wei, Chen, Guo, Zhang, Wang (b0105) 2015; 36 Brenner, Franz, Kühlenthal, Kuschnerus, Remm, Gross, Theiss, Landmesser, Kränkel (b0120) 2015; 199 Erbel, Tyka, Helmes, Akhavanpoor, Rupp, Domschke, Linden, Wolf, Doesch, Lasitschka, Katus, Gleissner (b0095) 2015; 21 Li, Lei, Cao, Mi, Li, Cao (b0100) 2018; 55 Gleissner, Shaked, Little, Ley (b0090) 2010; 184 Zhou, Chen, Liu, Wu, Guo, Lin (b0135) 2017; 15 H. Winkels, E. hinger, M. Vassallo, K. Buscher, H.Q. Dinh, K. Kobiyama, A.A.J. Hamers, C. Cochain, E. Vafadarnejad, A.E. Saliba, A. Zernecke, A.B. Pramod, A.K. Ghosh, N. Anto Michel, N. Hoppe, I. Hilgendorf, A. Zirlik, C.C. Hedrick, K. Ley, D. Wolf, Atlas of the immune cell repertoire in mouse atherosclerosis defined by single-cell RNA-sequencing and mass cytometry, Circ. Res. 122 (2018) 1675–1688. https://doi.org/10.1161/CIRCRESAHA.117.312513. Rinne, Guillamat-Prats, Rami, Bindila, Ring, Lyytikäinen, Raitoharju, Oksala, Lehtimäki, Weber, van der Vorst, Steffens (b0145) 2018; 38 Guo, Xiao, Sheng, Zhang, Tie, Wang, Zhao, Ji (b0115) 2018; 9 Van den Bossche, Baardman, Otto, van der Velden, Neele, van den Berg, Luque-Martin, Chen, Boshuizen, Ahmed, Hoeksema, de Vos, de Winther (b0185) 2016; 17 Chinetti-Gbaguidi, Daoudi, Rosa, Vinod, Louvet, Copin, Fanchon, Vanhoutte, Derudas, Belloy, Haulon, Zawadzki, Susen, Massy, Eeckhoute, Staels (b0035) 2017; 121 Erbel, Wolf, Lasitschka, Linden, Domschke, Akhavanpoor, Doesch, Katus, Gleissner (b0045) 2015; 186 Bruen, Curley, Kajani, Crean, O'Reilly, Lucitt, Godson, McGillicuddy, Belton (b0125) 2017; 16 Yin, You, Swier, Tang, Radwan, Pandya, Agrawal (b0150) 2015; 35 Stöger, Gijbels, van der Velden, Manca, van der Loos, Biessen, Daemen, Lutgens, de Winther (b0025) 2012; 225 Finn, Nakano, Polavarapu, Karmali, Saeed, Zhao, Yazdani, Otsuka, Davis, Habib, Narula, Kolodgie, Virmani (b0040) 2012; 59 Li, Sheng, Liu, Qian, Wu, Wu, Ma, Yao (b0140) 2019; 30 L.E. Otterbein, F.H. Bach, I. Alam, M. Soares, T.L.H.M. Wysk, R.J. Davis, R.A. Flavell, A.M. Choi, Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway, Nat Med. 6 (2000) 422–428. https://doi.org/10.1038/74680. Taguchi, Nagao, Maeda, Yanagisawa, Sakai, Yamasaki, Wakayama, Watanabe, Otagiri, Maruyama (b0195) 2018; 25 Tajbakhsh, Rezaee, Kovanen, Sahebkar (b0065) 2018; 188 Zhang, Huang, Li, Dang, Yuan, Wang, Zeng, Sun, Liu, Ao, Tan, Su, Qian, Olsen, Zheng (b0160) 2018; 9 Boyle, Johns, Kampfer, Nguyen, Game, Schaer, Mason, Haskard (b0085) 2012; 110 Wan, Huo, Johns, Piper, Mason, Carling, Haskard, Boyle (b0130) 2013; 33 P.J. Murray, J.E. Allen, S.K. Biswas, E.A. Fisher, D.W. Gilroy, S. Goerdt, S. Gordon, J.A. Hamilton, L.B. Ivashkiv, T. Lawrence, M. Locati, A. Mantovani, F.O. Martinez, J.L. Mege, D.M. Mosser, G. Natoli, J.P. Saeij, J.L. Schultze, K.A. Shirey, A. Sica, J. Suttles, I. Udalova, J.A. van Ginderachter, S.N. Vogel, T.A. Wynn, Macrophage activation and polarization: nomenclature and experimental guidelines, Immunity. 41 (2014) 14–20. https://doi.org/10.1016/j.immuni.2014.06.008. A. Kadl, A.K. Meher, P.R. Sharma, M.Y. Lee, A.C. Doran, S.R. Johnstone, M.R. Elliott, F. Gruber, J. Han, W. Chen, T. Kensler, K.S. Ravichandran, B.E. Isakson, B.R. Wamhoff, Leitinger. N, Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2, Circ Res. 107 (2010) 737–746. https://doi: 10.1161/CIRCRESAHA.109.215715. Kadl, Meher, Sharma, Lee, Doran, Johnstone, Elliott, Gruber, Han, Chen, Kensler, Ravichandran, Isakson, Wamhoff, Leitinger (b0020) 2010; 107 C. Ma, Q. Ouyang, Z. Huang, X. Chen, Y. Lin, W. Hu, L. Lin L, Toll-Like Receptor 9 Inactivation Alleviated Atherosclerotic Progression and Inhibited Macrophage Polarized to M1 Phenotype in ApoE-/- Mice, Dis Markers. 2015 (2015) 9. http://dx.doi.org/10.1155/2015/909572. Villa-Bellosta, Hamczyk, Andrés (b0075) 2016; 310 Zhang, Liu, Qiao, Zhang, Liu, Dong, Dai, Ni, Luan, Guan, Lu (b0110) 2018; 22 Chinetti-Gbaguidi, Baron, Bouhlel, Vanhoutte, Copin, Sebti, Derudas, Mayi, Bories, Tailleux, Haulon, Zawadzki, Jude, Staels (b0030) 2011; 108 Mallat, Gojova, Marchiol-Fournigault, Esposito, Kamaté, Merval, Fradelizi, Tedgui (b0060) 2001; 89 Lu, Zhang, Geng, Peng, Jayaraman, Chen, Xu, Yang, Li, Zheng, Shen, Wang, Liu, Wang, Zheng, Qi, Si, He, Liu, Lira, Sikora, Li, Xiong (b0180) 2015; 6 Shioi, Ikari (b0080) 2018; 25 Bisgaard, Mogensen, Rosendahl, Cucak, Nielsen, Rasmussen, Pedersen (b0055) 2016; 6 Boyle, Harrington, Piper, Elderfield, Stark, Landis, Haskard (b0015) 2009; 174 Rahman, Vengrenyuk, Ramsey, Vila, Girgis, Liu, Gusarova, Gromada, Weinstock, Moore, Loke, Fisher (b0070) 2017; 127 McAlpine, Huang, Emdin, Banko, Beriault, Shi, WerstucK (b0155) 2015; 35 Miao, Shen, Whiteman, Xin, Shen, Xin, Moore, Zhu (b0175) 2016; 25 Xu, Li, Wu, Shen, Ma, Qian, Ge (b0165) 2017; 37 Yin (10.1016/j.cca.2019.10.034_b0150) 2015; 35 Gleissner (10.1016/j.cca.2019.10.034_b0090) 2010; 184 10.1016/j.cca.2019.10.034_b0190 10.1016/j.cca.2019.10.034_b0050 Lu (10.1016/j.cca.2019.10.034_b0180) 2015; 6 10.1016/j.cca.2019.10.034_b0170 Taguchi (10.1016/j.cca.2019.10.034_b0195) 2018; 25 Villa-Bellosta (10.1016/j.cca.2019.10.034_b0075) 2016; 310 10.1016/j.cca.2019.10.034_b0010 Zhou (10.1016/j.cca.2019.10.034_b0105) 2015; 36 Mallat (10.1016/j.cca.2019.10.034_b0060) 2001; 89 Finn (10.1016/j.cca.2019.10.034_b0040) 2012; 59 Chinetti-Gbaguidi (10.1016/j.cca.2019.10.034_b0035) 2017; 121 Chinetti-Gbaguidi (10.1016/j.cca.2019.10.034_b0030) 2011; 108 Li (10.1016/j.cca.2019.10.034_b0140) 2019; 30 Kadl (10.1016/j.cca.2019.10.034_b0020) 2010; 107 Guo (10.1016/j.cca.2019.10.034_b0115) 2018; 9 Erbel (10.1016/j.cca.2019.10.034_b0045) 2015; 186 Zhang (10.1016/j.cca.2019.10.034_b0110) 2018; 22 Miao (10.1016/j.cca.2019.10.034_b0175) 2016; 25 Zhang (10.1016/j.cca.2019.10.034_b0160) 2018; 9 Bruen (10.1016/j.cca.2019.10.034_b0125) 2017; 16 10.1016/j.cca.2019.10.034_b0005 Li (10.1016/j.cca.2019.10.034_b0100) 2018; 55 Zhou (10.1016/j.cca.2019.10.034_b0135) 2017; 15 McAlpine (10.1016/j.cca.2019.10.034_b0155) 2015; 35 Shioi (10.1016/j.cca.2019.10.034_b0080) 2018; 25 Boyle (10.1016/j.cca.2019.10.034_b0085) 2012; 110 Xu (10.1016/j.cca.2019.10.034_b0165) 2017; 37 Brenner (10.1016/j.cca.2019.10.034_b0120) 2015; 199 Van den Bossche (10.1016/j.cca.2019.10.034_b0185) 2016; 17 Wan (10.1016/j.cca.2019.10.034_b0130) 2013; 33 Boyle (10.1016/j.cca.2019.10.034_b0015) 2009; 174 Tajbakhsh (10.1016/j.cca.2019.10.034_b0065) 2018; 188 Rinne (10.1016/j.cca.2019.10.034_b0145) 2018; 38 Stöger (10.1016/j.cca.2019.10.034_b0025) 2012; 225 Erbel (10.1016/j.cca.2019.10.034_b0095) 2015; 21 Rahman (10.1016/j.cca.2019.10.034_b0070) 2017; 127 Bisgaard (10.1016/j.cca.2019.10.034_b0055) 2016; 6 |
References_xml | – reference: H. Winkels, E. hinger, M. Vassallo, K. Buscher, H.Q. Dinh, K. Kobiyama, A.A.J. Hamers, C. Cochain, E. Vafadarnejad, A.E. Saliba, A. Zernecke, A.B. Pramod, A.K. Ghosh, N. Anto Michel, N. Hoppe, I. Hilgendorf, A. Zirlik, C.C. Hedrick, K. Ley, D. Wolf, Atlas of the immune cell repertoire in mouse atherosclerosis defined by single-cell RNA-sequencing and mass cytometry, Circ. Res. 122 (2018) 1675–1688. https://doi.org/10.1161/CIRCRESAHA.117.312513. – volume: 15 start-page: E358 year: 2017 ident: b0135 article-title: Asperlin Inhibits LPS-evoked foam cell formation and prevents atherosclerosis in ApoE−/−Mice publication-title: Mar. Drugs – volume: 21 start-page: 255 year: 2015 end-page: 265 ident: b0095 article-title: CXCL4-induced plaque macrophages can be specifically identified by co-expression of MMP7+S100A8+ in vitro and in vivo publication-title: Innate Immun. – volume: 25 start-page: 294 year: 2018 end-page: 303 ident: b0080 article-title: Plaque calcification during atherosclerosis progression and regression publication-title: J. Atheroscler. Thromb. – volume: 9 start-page: 464 year: 2018 ident: b0115 article-title: Ginsenoside Rg3 mitigates atherosclerosis progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype publication-title: Front. Pharmacol. – reference: P.J. Murray, J.E. Allen, S.K. Biswas, E.A. Fisher, D.W. Gilroy, S. Goerdt, S. Gordon, J.A. Hamilton, L.B. Ivashkiv, T. Lawrence, M. Locati, A. Mantovani, F.O. Martinez, J.L. Mege, D.M. Mosser, G. Natoli, J.P. Saeij, J.L. Schultze, K.A. Shirey, A. Sica, J. Suttles, I. Udalova, J.A. van Ginderachter, S.N. Vogel, T.A. Wynn, Macrophage activation and polarization: nomenclature and experimental guidelines, Immunity. 41 (2014) 14–20. https://doi.org/10.1016/j.immuni.2014.06.008. – volume: 30 start-page: 339 year: 2019 end-page: 351 ident: b0140 article-title: Kallistatin inhibits atherosclerotic inflammation by regulating macrophage polarization publication-title: Hum. Gene Ther. – volume: 188 start-page: 12 year: 2018 end-page: 25 ident: b0065 article-title: Efferocytosis in atherosclerotic lesions: malfunctioning regulatory pathways and control mechanisms publication-title: Pharmacol. Ther. – volume: 89 start-page: 930 year: 2001 end-page: 934 ident: b0060 article-title: Inhibition of transforming growth factor-beta signaling accelerates atherosclerosis and induces an unstable plaque phenotype in mice publication-title: Circ. Res. – volume: 127 start-page: 2904 year: 2017 end-page: 2915 ident: b0070 article-title: Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression publication-title: J. Clin. Invest. – volume: 110 start-page: 20 year: 2012 end-page: 33 ident: b0085 article-title: Activating transcription factor 1 directs Mhem atheroprotective macrophages through coordinated iron handling and foam cell protection publication-title: Circ. Res. – volume: 37 start-page: 226 year: 2017 end-page: 236 ident: b0165 article-title: Role of KCa3.1 channels in macrophage polarization and its relevance in atherosclerotic plaque instability publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 225 start-page: 461 year: 2012 end-page: 468 ident: b0025 article-title: Distribution of macrophage polarization markers in human atherosclerosis publication-title: Atherosclerosis – volume: 25 start-page: 268 year: 2016 end-page: 281 ident: b0175 article-title: Hydrogen sulfide mitigates myocardial infarction via promotion of mitochondrial biogenesis-Dependent M2 polarization of macrophages publication-title: Antioxid. Redox Signal. – volume: 17 start-page: 684 year: 2016 end-page: 696 ident: b0185 article-title: Mitochondrial dysfunction prevents repolarization of inflammatory macrophages publication-title: Cell Rep. – volume: 55 start-page: 120 year: 2018 end-page: 127 ident: b0100 article-title: Crocin alleviates coronary atherosclerosis via inhibiting lipid synthesis and inducing M2 macrophage polarization publication-title: Int. Immunopharmacol. – volume: 59 start-page: 166 year: 2012 end-page: 177 ident: b0040 article-title: Hemoglobin directs macrophage differentiation and prevents foam cell formation in human atherosclerotic plaques publication-title: J. Am. Coll. Cardiol. – volume: 6 start-page: 35234 year: 2016 ident: b0055 article-title: Bone marrow-derived and peritoneal macrophages have different inflammatory response to oxLDL and M1/M2 marker expression - implications for atherosclerosis research publication-title: Sci. Rep. – volume: 121 start-page: 19 year: 2017 end-page: 30 ident: b0035 article-title: Human alternative macrophages populate calcified areas of atherosclerotic lesions and display impaired RANKL-Induced Osteoclastic Bone Resorption Activity publication-title: Circ. Res. – volume: 108 start-page: 985 year: 2011 end-page: 995 ident: b0030 article-title: Human atherosclerotic plaque alternative macrophages display low cholesterol handling but high phagocytosis because of distinct activities of the PPARγ and LXRα pathways publication-title: Circ. Res. – volume: 36 start-page: 631 year: 2015 end-page: 641 ident: b0105 article-title: Curcumin modulates macrophage polarization through the Inhibition of the Toll-Like Receptor 4 Expression and its Signaling Pathways publication-title: Cell Physiol. Biochem. – volume: 174 start-page: 1097 year: 2009 end-page: 1108 ident: b0015 article-title: Coronary intraplaque hemorrhage evokes a novel atheroprotective macrophage phenotype publication-title: Am. J. Pathol. – reference: A. Kadl, A.K. Meher, P.R. Sharma, M.Y. Lee, A.C. Doran, S.R. Johnstone, M.R. Elliott, F. Gruber, J. Han, W. Chen, T. Kensler, K.S. Ravichandran, B.E. Isakson, B.R. Wamhoff, Leitinger. N, Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2, Circ Res. 107 (2010) 737–746. https://doi: 10.1161/CIRCRESAHA.109.215715. – volume: 22 start-page: 409 year: 2018 end-page: 416 ident: b0110 article-title: Ginsenoside Rb1 enhances atherosclerotic plaque stability by skewing macrophages to the M2 phenotype publication-title: J. Cell. Mol. Med. – volume: 9 start-page: 878 year: 2018 ident: b0160 article-title: Human Gingiva-Derived Mesenchymal stem cells modulate monocytes/macrophages and alleviate Atherosclerosis publication-title: Front. Immunol. – reference: L.E. Otterbein, F.H. Bach, I. Alam, M. Soares, T.L.H.M. Wysk, R.J. Davis, R.A. Flavell, A.M. Choi, Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway, Nat Med. 6 (2000) 422–428. https://doi.org/10.1038/74680. – volume: 35 start-page: 2432 year: 2015 end-page: 2442 ident: b0150 article-title: Vitamin D protects against atherosclerosis via regulation of cholesterol efflux and macrophage polarization in hypercholesterolemic Swine publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 107 start-page: 737 year: 2010 end-page: 746 ident: b0020 article-title: Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2 publication-title: Circ. Res. – volume: 16 start-page: 143 year: 2017 ident: b0125 article-title: Liraglutide dictates macrophage phenotype in apolipoprotein E null mice during early atherosclerosis publication-title: Cardiovasc. Diabetol. – reference: C. Ma, Q. Ouyang, Z. Huang, X. Chen, Y. Lin, W. Hu, L. Lin L, Toll-Like Receptor 9 Inactivation Alleviated Atherosclerotic Progression and Inhibited Macrophage Polarized to M1 Phenotype in ApoE-/- Mice, Dis Markers. 2015 (2015) 9. http://dx.doi.org/10.1155/2015/909572. – volume: 33 start-page: 2470 year: 2013 end-page: 2480 ident: b0130 article-title: 5'-AMP-activated protein kinase-activating transcription factor 1 cascade modulates human monocyte-derived macrophages to atheroprotective functions in response to heme or metformin publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 184 start-page: 4810 year: 2010 end-page: 4818 ident: b0090 article-title: CXC chemokine ligand 4 induces a unique transcriptome in monocyte-derived macrophages publication-title: J Immunol. – volume: 38 start-page: 2562 year: 2018 end-page: 2575 ident: b0145 article-title: Palmitoylethanolamide promotes a proresolving macrophage phenotype and attenuates atherosclerotic plaque formation publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 6 start-page: 6676 year: 2015 ident: b0180 article-title: Myeloid cell-derived inducible nitric oxide synthase suppresses M1 macrophage polarization publication-title: Nat. Commun. – volume: 25 start-page: 1266 year: 2018 end-page: 1274 ident: b0195 article-title: Biomimetic carbon monoxide delivery based on hemoglobin vesicles ameliorates acute pancreatitis in mice via the regulation of macrophage and neutrophil activity publication-title: Drug Deliv. – volume: 35 start-page: 1113 year: 2015 end-page: 1122 ident: b0155 article-title: Deletion of Myeloid GSK3α attenuates atherosclerosis and promotes an M2 macrophage phenotype publication-title: Arterioscler. Thromb. Vasc. Biol. – volume: 310 start-page: C788 year: 2016 end-page: C799 ident: b0075 article-title: Alternatively activated macrophages exhibit an anticalcifying activity dependent on extracellular ATP/pyrophosphate metabolism publication-title: Am. J. Physiol. Cell Physiol. – volume: 186 start-page: 219 year: 2015 end-page: 225 ident: b0045 article-title: Prevalence of M4 macrophages within human coronary atherosclerotic plaques is associated with features of plaque instability publication-title: Int. J. Cardiol. – volume: 199 start-page: 163 year: 2015 end-page: 169 ident: b0120 article-title: DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages publication-title: Int. J. Cardiol. – volume: 35 start-page: 2432 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0150 article-title: Vitamin D protects against atherosclerosis via regulation of cholesterol efflux and macrophage polarization in hypercholesterolemic Swine publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.115.306132 – volume: 9 start-page: 464 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0115 article-title: Ginsenoside Rg3 mitigates atherosclerosis progression in Diabetic apoE–/– Mice by Skewing Macrophages to the M2 Phenotype publication-title: Front. Pharmacol. doi: 10.3389/fphar.2018.00464 – volume: 25 start-page: 268 year: 2016 ident: 10.1016/j.cca.2019.10.034_b0175 article-title: Hydrogen sulfide mitigates myocardial infarction via promotion of mitochondrial biogenesis-Dependent M2 polarization of macrophages publication-title: Antioxid. Redox Signal. doi: 10.1089/ars.2015.6577 – volume: 36 start-page: 631 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0105 article-title: Curcumin modulates macrophage polarization through the Inhibition of the Toll-Like Receptor 4 Expression and its Signaling Pathways publication-title: Cell Physiol. Biochem. doi: 10.1159/000430126 – volume: 25 start-page: 294 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0080 article-title: Plaque calcification during atherosclerosis progression and regression publication-title: J. Atheroscler. Thromb. doi: 10.5551/jat.RV17020 – volume: 186 start-page: 219 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0045 article-title: Prevalence of M4 macrophages within human coronary atherosclerotic plaques is associated with features of plaque instability publication-title: Int. J. Cardiol. doi: 10.1016/j.ijcard.2015.03.151 – volume: 35 start-page: 1113 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0155 article-title: Deletion of Myeloid GSK3α attenuates atherosclerosis and promotes an M2 macrophage phenotype publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.115.305438 – volume: 55 start-page: 120 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0100 article-title: Crocin alleviates coronary atherosclerosis via inhibiting lipid synthesis and inducing M2 macrophage polarization publication-title: Int. Immunopharmacol. doi: 10.1016/j.intimp.2017.11.037 – volume: 6 start-page: 6676 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0180 article-title: Myeloid cell-derived inducible nitric oxide synthase suppresses M1 macrophage polarization publication-title: Nat. Commun. doi: 10.1038/ncomms7676 – volume: 174 start-page: 1097 year: 2009 ident: 10.1016/j.cca.2019.10.034_b0015 article-title: Coronary intraplaque hemorrhage evokes a novel atheroprotective macrophage phenotype publication-title: Am. J. Pathol. doi: 10.2353/ajpath.2009.080431 – volume: 16 start-page: 143 year: 2017 ident: 10.1016/j.cca.2019.10.034_b0125 article-title: Liraglutide dictates macrophage phenotype in apolipoprotein E null mice during early atherosclerosis publication-title: Cardiovasc. Diabetol. doi: 10.1186/s12933-017-0626-3 – volume: 59 start-page: 166 year: 2012 ident: 10.1016/j.cca.2019.10.034_b0040 article-title: Hemoglobin directs macrophage differentiation and prevents foam cell formation in human atherosclerotic plaques publication-title: J. Am. Coll. Cardiol. doi: 10.1016/j.jacc.2011.10.852 – volume: 107 start-page: 737 year: 2010 ident: 10.1016/j.cca.2019.10.034_b0020 article-title: Identification of a novel macrophage phenotype that develops in response to atherogenic phospholipids via Nrf2 publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.109.215715 – volume: 38 start-page: 2562 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0145 article-title: Palmitoylethanolamide promotes a proresolving macrophage phenotype and attenuates atherosclerotic plaque formation publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.118.311185 – volume: 6 start-page: 35234 year: 2016 ident: 10.1016/j.cca.2019.10.034_b0055 article-title: Bone marrow-derived and peritoneal macrophages have different inflammatory response to oxLDL and M1/M2 marker expression - implications for atherosclerosis research publication-title: Sci. Rep. doi: 10.1038/srep35234 – ident: 10.1016/j.cca.2019.10.034_b0005 doi: 10.1161/CIRCRESAHA.117.312513 – ident: 10.1016/j.cca.2019.10.034_b0190 doi: 10.1038/74680 – volume: 30 start-page: 339 year: 2019 ident: 10.1016/j.cca.2019.10.034_b0140 article-title: Kallistatin inhibits atherosclerotic inflammation by regulating macrophage polarization publication-title: Hum. Gene Ther. doi: 10.1089/hum.2018.084 – volume: 25 start-page: 1266 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0195 article-title: Biomimetic carbon monoxide delivery based on hemoglobin vesicles ameliorates acute pancreatitis in mice via the regulation of macrophage and neutrophil activity publication-title: Drug Deliv. doi: 10.1080/10717544.2018.1477860 – volume: 188 start-page: 12 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0065 article-title: Efferocytosis in atherosclerotic lesions: malfunctioning regulatory pathways and control mechanisms publication-title: Pharmacol. Ther. doi: 10.1016/j.pharmthera.2018.02.003 – volume: 310 start-page: C788 year: 2016 ident: 10.1016/j.cca.2019.10.034_b0075 article-title: Alternatively activated macrophages exhibit an anticalcifying activity dependent on extracellular ATP/pyrophosphate metabolism publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00370.2015 – volume: 199 start-page: 163 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0120 article-title: DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages publication-title: Int. J. Cardiol. doi: 10.1016/j.ijcard.2015.07.044 – ident: 10.1016/j.cca.2019.10.034_b0050 doi: 10.1161/CIRCRESAHA.109.215715 – volume: 21 start-page: 255 year: 2015 ident: 10.1016/j.cca.2019.10.034_b0095 article-title: CXCL4-induced plaque macrophages can be specifically identified by co-expression of MMP7+S100A8+ in vitro and in vivo publication-title: Innate Immun. doi: 10.1177/1753425914526461 – ident: 10.1016/j.cca.2019.10.034_b0170 doi: 10.1155/2015/909572 – volume: 33 start-page: 2470 year: 2013 ident: 10.1016/j.cca.2019.10.034_b0130 article-title: 5'-AMP-activated protein kinase-activating transcription factor 1 cascade modulates human monocyte-derived macrophages to atheroprotective functions in response to heme or metformin publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.113.300986 – volume: 15 start-page: E358 year: 2017 ident: 10.1016/j.cca.2019.10.034_b0135 article-title: Asperlin Inhibits LPS-evoked foam cell formation and prevents atherosclerosis in ApoE−/−Mice publication-title: Mar. Drugs doi: 10.3390/md15110358 – ident: 10.1016/j.cca.2019.10.034_b0010 doi: 10.1016/j.immuni.2014.06.008 – volume: 9 start-page: 878 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0160 article-title: Human Gingiva-Derived Mesenchymal stem cells modulate monocytes/macrophages and alleviate Atherosclerosis publication-title: Front. Immunol. doi: 10.3389/fimmu.2018.00878 – volume: 89 start-page: 930 year: 2001 ident: 10.1016/j.cca.2019.10.034_b0060 article-title: Inhibition of transforming growth factor-beta signaling accelerates atherosclerosis and induces an unstable plaque phenotype in mice publication-title: Circ. Res. doi: 10.1161/hh2201.099415 – volume: 22 start-page: 409 year: 2018 ident: 10.1016/j.cca.2019.10.034_b0110 article-title: Ginsenoside Rb1 enhances atherosclerotic plaque stability by skewing macrophages to the M2 phenotype publication-title: J. Cell. Mol. Med. doi: 10.1111/jcmm.13329 – volume: 127 start-page: 2904 year: 2017 ident: 10.1016/j.cca.2019.10.034_b0070 article-title: Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression publication-title: J. Clin. Invest. doi: 10.1172/JCI75005 – volume: 37 start-page: 226 year: 2017 ident: 10.1016/j.cca.2019.10.034_b0165 article-title: Role of KCa3.1 channels in macrophage polarization and its relevance in atherosclerotic plaque instability publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/ATVBAHA.116.308461 – volume: 225 start-page: 461 year: 2012 ident: 10.1016/j.cca.2019.10.034_b0025 article-title: Distribution of macrophage polarization markers in human atherosclerosis publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2012.09.013 – volume: 17 start-page: 684 year: 2016 ident: 10.1016/j.cca.2019.10.034_b0185 article-title: Mitochondrial dysfunction prevents repolarization of inflammatory macrophages publication-title: Cell Rep. doi: 10.1016/j.celrep.2016.09.008 – volume: 184 start-page: 4810 year: 2010 ident: 10.1016/j.cca.2019.10.034_b0090 article-title: CXC chemokine ligand 4 induces a unique transcriptome in monocyte-derived macrophages publication-title: J Immunol. doi: 10.4049/jimmunol.0901368 – volume: 121 start-page: 19 year: 2017 ident: 10.1016/j.cca.2019.10.034_b0035 article-title: Human alternative macrophages populate calcified areas of atherosclerotic lesions and display impaired RANKL-Induced Osteoclastic Bone Resorption Activity publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.116.310262 – volume: 110 start-page: 20 year: 2012 ident: 10.1016/j.cca.2019.10.034_b0085 article-title: Activating transcription factor 1 directs Mhem atheroprotective macrophages through coordinated iron handling and foam cell protection publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.111.247577 – volume: 108 start-page: 985 year: 2011 ident: 10.1016/j.cca.2019.10.034_b0030 article-title: Human atherosclerotic plaque alternative macrophages display low cholesterol handling but high phagocytosis because of distinct activities of the PPARγ and LXRα pathways publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.110.233775 |
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Snippet | •Effects of macrophages on atherosclerosis are related to macrophage polarization.•Different macrophage phenotypes have different effects on the plaque... Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis... |
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Title | Macrophage polarization in atherosclerosis |
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