Inhibitory effect of (pro)renin receptor decoy inhibitor PRO20 on endoplasmic reticulum stress during cardiac remodeling
Background: Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling...
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| Published in | Frontiers in pharmacology Vol. 13; p. 940365 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Frontiers Media S.A
12.08.2022
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| Subjects | |
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| Abstract | Background:
Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling and heart failure remains unknown.
Materials and methods:
Transverse aortic constriction (TAC) surgery was performed to establish a mouse model of chronic pressure overload-induced cardiac remodeling. Neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were isolated and stimulated by Angiotensin II (Ang II). PRR decoy inhibitor PRO20 was synthesized and used to evaluate its effect on cardiac remodeling.
Results:
Soluble PRR and PRR were significantly upregulated in TAC-induced cardiac remodeling and Ang II-treated CMs and CFs. Results of
In vivo
experiments showed that suppression of PRR by PRO20 significantly retarded cardiac remodeling and heart failure indicated by morphological and echocardiographic analyses.
In vitro
experiments, PRO20 inhibited CM hypertrophy, and also alleviated CF activation, proliferation and extracellular matrix synthesis. Mechanically, PRO20 enhanced intracellular cAMP levels, but not affected cGMP levels in CMs and CFs. Moreover, treatment of PRO20 in CFs markedly attenuated the production of reactive oxygen species and phosphorylation of IRE1 and PERK, two well-identified markers of endoplasmic reticulum (ER) stress. Accordingly, administration of PRO20 reversed ER stressor thapsigargin-induced CM hypertrophy and CF activation/migration.
Conclusion:
Taken together, these findings suggest that inhibition of PRR by PRO20 attenuates cardiac remodeling through increasing cAMP levels and reducing ER stress in both CMs and CFs. |
|---|---|
| AbstractList | Background:
Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling and heart failure remains unknown.
Materials and methods:
Transverse aortic constriction (TAC) surgery was performed to establish a mouse model of chronic pressure overload-induced cardiac remodeling. Neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were isolated and stimulated by Angiotensin II (Ang II). PRR decoy inhibitor PRO20 was synthesized and used to evaluate its effect on cardiac remodeling.
Results:
Soluble PRR and PRR were significantly upregulated in TAC-induced cardiac remodeling and Ang II-treated CMs and CFs. Results of
In vivo
experiments showed that suppression of PRR by PRO20 significantly retarded cardiac remodeling and heart failure indicated by morphological and echocardiographic analyses.
In vitro
experiments, PRO20 inhibited CM hypertrophy, and also alleviated CF activation, proliferation and extracellular matrix synthesis. Mechanically, PRO20 enhanced intracellular cAMP levels, but not affected cGMP levels in CMs and CFs. Moreover, treatment of PRO20 in CFs markedly attenuated the production of reactive oxygen species and phosphorylation of IRE1 and PERK, two well-identified markers of endoplasmic reticulum (ER) stress. Accordingly, administration of PRO20 reversed ER stressor thapsigargin-induced CM hypertrophy and CF activation/migration.
Conclusion:
Taken together, these findings suggest that inhibition of PRR by PRO20 attenuates cardiac remodeling through increasing cAMP levels and reducing ER stress in both CMs and CFs. Background: Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling and heart failure remains unknown.Materials and methods: Transverse aortic constriction (TAC) surgery was performed to establish a mouse model of chronic pressure overload-induced cardiac remodeling. Neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were isolated and stimulated by Angiotensin II (Ang II). PRR decoy inhibitor PRO20 was synthesized and used to evaluate its effect on cardiac remodeling.Results: Soluble PRR and PRR were significantly upregulated in TAC-induced cardiac remodeling and Ang II-treated CMs and CFs. Results of In vivo experiments showed that suppression of PRR by PRO20 significantly retarded cardiac remodeling and heart failure indicated by morphological and echocardiographic analyses. In vitro experiments, PRO20 inhibited CM hypertrophy, and also alleviated CF activation, proliferation and extracellular matrix synthesis. Mechanically, PRO20 enhanced intracellular cAMP levels, but not affected cGMP levels in CMs and CFs. Moreover, treatment of PRO20 in CFs markedly attenuated the production of reactive oxygen species and phosphorylation of IRE1 and PERK, two well-identified markers of endoplasmic reticulum (ER) stress. Accordingly, administration of PRO20 reversed ER stressor thapsigargin-induced CM hypertrophy and CF activation/migration.Conclusion: Taken together, these findings suggest that inhibition of PRR by PRO20 attenuates cardiac remodeling through increasing cAMP levels and reducing ER stress in both CMs and CFs. Background: Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling and heart failure remains unknown. Materials and methods: Transverse aortic constriction (TAC) surgery was performed to establish a mouse model of chronic pressure overload-induced cardiac remodeling. Neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were isolated and stimulated by Angiotensin II (Ang II). PRR decoy inhibitor PRO20 was synthesized and used to evaluate its effect on cardiac remodeling. Results: Soluble PRR and PRR were significantly upregulated in TAC-induced cardiac remodeling and Ang II-treated CMs and CFs. Results of In vivo experiments showed that suppression of PRR by PRO20 significantly retarded cardiac remodeling and heart failure indicated by morphological and echocardiographic analyses. In vitro experiments, PRO20 inhibited CM hypertrophy, and also alleviated CF activation, proliferation and extracellular matrix synthesis. Mechanically, PRO20 enhanced intracellular cAMP levels, but not affected cGMP levels in CMs and CFs. Moreover, treatment of PRO20 in CFs markedly attenuated the production of reactive oxygen species and phosphorylation of IRE1 and PERK, two well-identified markers of endoplasmic reticulum (ER) stress. Accordingly, administration of PRO20 reversed ER stressor thapsigargin-induced CM hypertrophy and CF activation/migration. Conclusion: Taken together, these findings suggest that inhibition of PRR by PRO20 attenuates cardiac remodeling through increasing cAMP levels and reducing ER stress in both CMs and CFs.Background: Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and prorenin, participating in the progression of nephrology. However, whether PRR could be considered as a therapeutic target for cardiac remodeling and heart failure remains unknown. Materials and methods: Transverse aortic constriction (TAC) surgery was performed to establish a mouse model of chronic pressure overload-induced cardiac remodeling. Neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) were isolated and stimulated by Angiotensin II (Ang II). PRR decoy inhibitor PRO20 was synthesized and used to evaluate its effect on cardiac remodeling. Results: Soluble PRR and PRR were significantly upregulated in TAC-induced cardiac remodeling and Ang II-treated CMs and CFs. Results of In vivo experiments showed that suppression of PRR by PRO20 significantly retarded cardiac remodeling and heart failure indicated by morphological and echocardiographic analyses. In vitro experiments, PRO20 inhibited CM hypertrophy, and also alleviated CF activation, proliferation and extracellular matrix synthesis. Mechanically, PRO20 enhanced intracellular cAMP levels, but not affected cGMP levels in CMs and CFs. Moreover, treatment of PRO20 in CFs markedly attenuated the production of reactive oxygen species and phosphorylation of IRE1 and PERK, two well-identified markers of endoplasmic reticulum (ER) stress. Accordingly, administration of PRO20 reversed ER stressor thapsigargin-induced CM hypertrophy and CF activation/migration. Conclusion: Taken together, these findings suggest that inhibition of PRR by PRO20 attenuates cardiac remodeling through increasing cAMP levels and reducing ER stress in both CMs and CFs. |
| Author | Zhang, Jing Luo, Chang-Jun Cheng, Yun-Jiu Yu, Jia |
| AuthorAffiliation | 3 Department of General Practice School , Guangxi Medical University , Nanning , China 2 Department of Cardiology , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , China 1 Department of Cardiology , Liuzhou Municipal Liutie Central Hospital , Liuzhou , China |
| AuthorAffiliation_xml | – name: 2 Department of Cardiology , The First Affiliated Hospital of Sun Yat-sen University , Guangzhou , China – name: 1 Department of Cardiology , Liuzhou Municipal Liutie Central Hospital , Liuzhou , China – name: 3 Department of General Practice School , Guangxi Medical University , Nanning , China |
| Author_xml | – sequence: 1 givenname: Jing surname: Zhang fullname: Zhang, Jing – sequence: 2 givenname: Yun-Jiu surname: Cheng fullname: Cheng, Yun-Jiu – sequence: 3 givenname: Chang-Jun surname: Luo fullname: Luo, Chang-Jun – sequence: 4 givenname: Jia surname: Yu fullname: Yu, Jia |
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| CitedBy_id | crossref_primary_10_1111_1440_1681_13802 crossref_primary_10_1038_s41440_023_01424_6 crossref_primary_10_3389_fcvm_2023_1086603 crossref_primary_10_1007_s11010_024_05014_z crossref_primary_10_2174_0113894501250617231016052930 |
| Cites_doi | 10.1161/CIRCHEARTFAILURE.120.007300 10.1111/j.1582-4934.2011.01374.x 10.3389/fphys.2022.784521 10.1038/nature17041 10.1111/bph.13888 10.1007/s10557-020-06959-1 10.1093/cvr/cvaa324 10.1073/pnas.1602397113 10.1007/s00018-016-2373-0 10.1161/HYPERTENSIONAHA.111.186056 10.1152/ajprenal.00405.2005 10.1042/CS20171167 10.1152/ajprenal.00071.2018 10.1161/HYPERTENSIONAHA.114.04458 10.1007/s11897-021-00501-6 10.1139/cjpp-2021-0260 10.1080/17460441.2020.1821643 10.1152/ajpregu.00319.2014 10.1038/s41581-021-00414-6 10.3389/fcell.2019.00249 10.1161/HYPERTENSIONAHA.120.15100 10.1152/ajpregu.00259.2020 10.1161/HYPERTENSIONAHA.114.03811 10.1007/164_2016_5007 10.1038/srep33678 10.1016/j.devcel.2007.07.018 10.1096/fj.202001711R 10.1111/j.1582-4934.2011.01377.x 10.1161/JAHA.113.000536 10.1152/ajprenal.00112.2020 10.3389/fcvm.2017.00029 10.1161/CIRCULATIONAHA.119.042178 10.1152/ajpcell.1994.266.6.C1603 10.1038/cdd.2016.138 10.1016/j.cardfail.2015.08.341 10.7150/ijbs.47180 10.1152/ajpcell.00191.2016 10.4172/jcs.1000111 10.1016/j.biopha.2020.110022 10.3390/ijms22084035 10.1172/jci.insight.124174 10.1042/CS20201047 10.1016/j.peptides.2018.04.010 10.1016/j.yjmcc.2019.01.025 10.3892/ijmm.2017.2856 10.1101/gad.964702 10.1074/jbc.RA119.007648 10.1093/cvr/cvaa233 10.1152/ajpheart.00373.2017 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Cardiovascular and Smooth Muscle Pharmacology, a section of the journal Frontiers in Pharmacology Reviewed by: Shengyu Mu, University of Arkansas for Medical Sciences, United States Venkatesh Katari, University of Toledo, United States Edited by: Guixue Wang, Chongqing University, China |
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| References | Fu (B16) 2021; 135 Feng (B14) 2021; 77 Arthur (B2) 2021; 320 Yang (B46) 2020; 16 Haque (B19) 2017; 74 Yuan (B48) 2019; 7 Wolter (B42) 2017; 238 Yang (B47) 2017; 39 Chen (B6) 2020; 141 Lu (B28) 2016; 113 Wang (B39) 2019; 4 Zhang (B50) 2020; 125 Li (B24) 2015; 65 Yamamoto (B45) 2007; 13 Bektur Aykanat (B3) 2021; 99 Xu (B44) 2019; 128 Tripathi (B36) 2021; 22 Zhang (B49) 2017; 4 Dong (B10) 2019; 294 Vigil-Garcia (B37) 2021; 117 Huang (B21) 2012; 59 Prieto (B32) 2021; 17 Cano (B4) 1994; 266 Liu (B26) 2014; 64 Wang (B41) 2018; 175 Chen (B7) 2020; 34 Manerikar (B30) 1976; 26 Domenig (B9) 2016; 6 Richards (B34) 2021; 14 Chen (B5) 2021; 16 Wang (B40) 2016; 529 Abboud (B1) 2021; 18 Lee (B22) 2002; 16 Preedy (B31) 2020; 34 Lu (B27) 2022; 13 Li (B23) 2015; 309 Singh (B35) 2016; 1 Hennrikus (B20) 2018; 314 Frangogiannis (B15) 2021; 117 Mahmud (B29) 2012; 16 Crajoinas (B8) 2016; 311 Ellmers (B12) 2016; 22 Prola (B33) 2017; 24 Gong (B17) 2019; 111 Wang (B38) 2020; 319 Greene (B18) 2013; 2 Li (B25) 2006; 291 Fang (B13) 2018; 315 Doyle (B11) 2011; 15 Wu (B43) 2017; 131 |
| References_xml | – volume: 14 start-page: e007300 year: 2021 ident: B34 article-title: CRD-733, a novel PDE9 (phosphodiesterase 9) inhibitor, reverses pressure overload-induced heart failure publication-title: Circ. Heart Fail. doi: 10.1161/CIRCHEARTFAILURE.120.007300 – volume: 15 start-page: 2025 year: 2011 ident: B11 article-title: Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders publication-title: J. Cell. Mol. Med. doi: 10.1111/j.1582-4934.2011.01374.x – volume: 13 start-page: 784521 year: 2022 ident: B27 article-title: (Pro)renin receptor regulates phosphate homeostasis in rats via releasing fibroblast growth factor-23 publication-title: Front. Physiol. doi: 10.3389/fphys.2022.784521 – volume: 529 start-page: 326 year: 2016 ident: B40 article-title: Protein misfolding in the endoplasmic reticulum as a conduit to human disease publication-title: Nature doi: 10.1038/nature17041 – volume: 175 start-page: 1293 year: 2018 ident: B41 article-title: Endoplasmic reticulum stress in the heart: insights into mechanisms and drug targets publication-title: Br. J. Pharmacol. doi: 10.1111/bph.13888 – volume: 34 start-page: 401 year: 2020 ident: B31 article-title: Cardiac cyclic nucleotide phosphodiesterases: roles and therapeutic potential in heart failure publication-title: Cardiovasc. Drugs Ther. doi: 10.1007/s10557-020-06959-1 – volume: 117 start-page: 1450 year: 2021 ident: B15 article-title: Cardiac fibrosis publication-title: Cardiovasc. Res. doi: 10.1093/cvr/cvaa324 – volume: 113 start-page: E1898 year: 2016 ident: B28 article-title: Soluble (pro)renin receptor via beta-catenin enhances urine concentration capability as a target of liver X receptor publication-title: Proc. Natl. Acad. Sci. U. S. A. doi: 10.1073/pnas.1602397113 – volume: 74 start-page: 983 year: 2017 ident: B19 article-title: How cardiomyocytes sense pathophysiological stresses for cardiac remodeling publication-title: Cell. Mol. Life Sci. doi: 10.1007/s00018-016-2373-0 – volume: 59 start-page: 317 year: 2012 ident: B21 article-title: Sodium depletion enhances renal expression of (pro)renin receptor via cyclic GMP-protein kinase G signaling pathway publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.111.186056 – volume: 291 start-page: F375 year: 2006 ident: B25 article-title: AT1 receptor-mediated accumulation of extracellular angiotensin II in proximal tubule cells: role of cytoskeleton microtubules and tyrosine phosphatases publication-title: Am. J. Physiol. Ren. Physiol. doi: 10.1152/ajprenal.00405.2005 – volume: 131 start-page: 2319 year: 2017 ident: B43 article-title: Mechanisms contributing to cardiac remodelling publication-title: Clin. Sci. doi: 10.1042/CS20171167 – volume: 315 start-page: F1759 year: 2018 ident: B13 article-title: Role of (pro)renin receptor in albumin overload-induced nephropathy in rats publication-title: Am. J. Physiol. Ren. Physiol. doi: 10.1152/ajprenal.00071.2018 – volume: 65 start-page: 352 year: 2015 ident: B24 article-title: Intracerebroventricular infusion of the (Pro)renin receptor antagonist PRO20 attenuates deoxycorticosterone acetate-salt-induced hypertension publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.114.04458 – volume: 18 start-page: 71 year: 2021 ident: B1 article-title: Reverse cardiac remodeling and ARNI therapy publication-title: Curr. Heart Fail. Rep. doi: 10.1007/s11897-021-00501-6 – volume: 99 start-page: 1226 year: 2021 ident: B3 article-title: Cardiac hypertrophy caused by hyperthyroidism in rats: the role of ATF-6 and TRPC1 channels publication-title: Can. J. Physiol. Pharmacol. doi: 10.1139/cjpp-2021-0260 – volume: 16 start-page: 183 year: 2021 ident: B5 article-title: An update of cyclic nucleotide phosphodiesterase as a target for cardiac diseases publication-title: Expert Opin. Drug Discov. doi: 10.1080/17460441.2020.1821643 – volume: 309 start-page: R138 year: 2015 ident: B23 article-title: Angiotensin II regulates brain (pro)renin receptor expression through activation of cAMP response element-binding protein publication-title: Am. J. Physiol. Regul. Integr. Comp. Physiol. doi: 10.1152/ajpregu.00319.2014 – volume: 17 start-page: 481 year: 2021 ident: B32 article-title: The evolving complexity of the collecting duct renin-angiotensin system in hypertension publication-title: Nat. Rev. Nephrol. doi: 10.1038/s41581-021-00414-6 – volume: 7 start-page: 249 year: 2019 ident: B48 article-title: MiR-144-3p enhances cardiac fibrosis after myocardial infarction by targeting PTEN publication-title: Front. Cell Dev. Biol. doi: 10.3389/fcell.2019.00249 – volume: 77 start-page: 405 year: 2021 ident: B14 article-title: Site-1 protease-derived soluble (Pro)Renin receptor contributes to angiotensin II-induced hypertension in mice publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.120.15100 – volume: 320 start-page: R377 year: 2021 ident: B2 article-title: (Pro)renin receptor in the kidney: function and significance publication-title: Am. J. Physiol. Regul. Integr. Comp. Physiol. doi: 10.1152/ajpregu.00259.2020 – volume: 64 start-page: 738 year: 2014 ident: B26 article-title: Endoplasmic reticulum stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) protects against pressure overload-induced heart failure and lung remodeling publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.114.03811 – volume: 26 start-page: 173 year: 1976 ident: B30 article-title: Immune status and BCG vaccination in newborns with intra-uterine growth retardation publication-title: Clin. Exp. Immunol. – volume: 238 start-page: 25 year: 2017 ident: B42 article-title: cCMP and cUMP in apoptosis: concepts and methods publication-title: Handb. Exp. Pharmacol. doi: 10.1007/164_2016_5007 – volume: 6 start-page: 33678 year: 2016 ident: B9 article-title: Neprilysin is a mediator of alternative renin-angiotensin-system Activation in the murine and human kidney publication-title: Sci. Rep. doi: 10.1038/srep33678 – volume: 13 start-page: 365 year: 2007 ident: B45 article-title: Transcriptional induction of mammalian ER quality control proteins is mediated by single or combined action of ATF6alpha and XBP1 publication-title: Dev. Cell doi: 10.1016/j.devcel.2007.07.018 – volume: 34 start-page: 14136 year: 2020 ident: B7 article-title: The interaction partners of (pro)renin receptor in the distal nephron publication-title: FASEB J. doi: 10.1096/fj.202001711R – volume: 16 start-page: 722 year: 2012 ident: B29 article-title: Regulation of the (pro)renin-renin receptor in cardiac remodelling publication-title: J. Cell. Mol. Med. doi: 10.1111/j.1582-4934.2011.01377.x – volume: 2 start-page: e000536 year: 2013 ident: B18 article-title: The cGMP signaling pathway as a therapeutic target in heart failure with preserved ejection fraction publication-title: J. Am. Heart Assoc. doi: 10.1161/JAHA.113.000536 – volume: 319 start-page: F647 year: 2020 ident: B38 article-title: COX-2-independent activation of renal (pro)renin receptor contributes to DOCA-salt hypertension in rats publication-title: Am. J. Physiol. Ren. Physiol. doi: 10.1152/ajprenal.00112.2020 – volume: 4 start-page: 29 year: 2017 ident: B49 article-title: Role of endoplasmic reticulum stress, autophagy, and inflammation in cardiovascular disease publication-title: Front. Cardiovasc. Med. doi: 10.3389/fcvm.2017.00029 – volume: 141 start-page: 217 year: 2020 ident: B6 article-title: A novel role of cyclic nucleotide phosphodiesterase 10A in pathological cardiac remodeling and dysfunction publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.119.042178 – volume: 266 start-page: C1603 year: 1994 ident: B4 article-title: Angiotensin II stimulation of Na-H antiporter activity is cAMP independent in OKP cells publication-title: Am. J. Physiol. doi: 10.1152/ajpcell.1994.266.6.C1603 – volume: 24 start-page: 343 year: 2017 ident: B33 article-title: SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation. publication-title: Cell Death Differ. doi: 10.1038/cdd.2016.138 – volume: 22 start-page: 64 year: 2016 ident: B12 article-title: (Pro)renin receptor blockade ameliorates cardiac injury and remodeling and improves function after myocardial infarction publication-title: J. Card. Fail. doi: 10.1016/j.cardfail.2015.08.341 – volume: 16 start-page: 2414 year: 2020 ident: B46 article-title: The roles of noncardiomyocytes in cardiac remodeling publication-title: Int. J. Biol. Sci. doi: 10.7150/ijbs.47180 – volume: 311 start-page: C768 year: 2016 ident: B8 article-title: Angiotensin II counteracts the effects of cAMP/PKA on NHE3 activity and phosphorylation in proximal tubule cells publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00191.2016 – volume: 1 start-page: 111 year: 2016 ident: B35 article-title: Angiotensin receptors: structure, function, signaling and clinical applications publication-title: J. Cell Signal. doi: 10.4172/jcs.1000111 – volume: 125 start-page: 110022 year: 2020 ident: B50 article-title: STING is an essential regulator of heart inflammation and fibrosis in mice with pathological cardiac hypertrophy via endoplasmic reticulum (ER) stress publication-title: Biomed. Pharmacother. doi: 10.1016/j.biopha.2020.110022 – volume: 22 start-page: 4035 year: 2021 ident: B36 article-title: A low-sodium diet boosts Ang (1-7) production and NO-cGMP bioavailability to reduce edema and enhance survival in experimental heart failure publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms22084035 – volume: 4 start-page: 124174 year: 2019 ident: B39 article-title: Site-1 protease-derived soluble (pro)renin receptor targets vasopressin receptor 2 to enhance urine concentrating capability publication-title: JCI Insight doi: 10.1172/jci.insight.124174 – volume: 135 start-page: 793 year: 2021 ident: B16 article-title: Soluble (pro)renin receptor induces endothelial dysfunction and hypertension in mice with diet-induced obesity via activation of angiotensin II type 1 receptor publication-title: Clin. Sci. doi: 10.1042/CS20201047 – volume: 111 start-page: 152 year: 2019 ident: B17 article-title: Elevated plasma soluble (pro)renin receptor levels are associated with left ventricular remodeling and renal function in chronic heart failure patients with reduced ejection fraction publication-title: Peptides doi: 10.1016/j.peptides.2018.04.010 – volume: 128 start-page: 105 year: 2019 ident: B44 article-title: Novel role of mitochondrial GTPases 1 in pathological cardiac hypertrophy publication-title: J. Mol. Cell. Cardiol. doi: 10.1016/j.yjmcc.2019.01.025 – volume: 39 start-page: 613 year: 2017 ident: B47 article-title: Renin-angiotensin system activation accelerates atherosclerosis in experimental renal failure by promoting endoplasmic reticulum stress-related inflammation publication-title: Int. J. Mol. Med. doi: 10.3892/ijmm.2017.2856 – volume: 16 start-page: 452 year: 2002 ident: B22 article-title: IRE1-mediated unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge to regulate XBP1 in signaling the unfolded protein response publication-title: Genes Dev. doi: 10.1101/gad.964702 – volume: 294 start-page: 8218 year: 2019 ident: B10 article-title: (Pro)renin receptor-mediated myocardial injury, apoptosis, and inflammatory response in rats with diabetic cardiomyopathy publication-title: J. Biol. Chem. doi: 10.1074/jbc.RA119.007648 – volume: 117 start-page: 1532 year: 2021 ident: B37 article-title: Gene expression profiling of hypertrophic cardiomyocytes identifies new players in pathological remodelling publication-title: Cardiovasc. Res. doi: 10.1093/cvr/cvaa233 – volume: 314 start-page: H139 year: 2018 ident: B20 article-title: The prorenin receptor in the cardiovascular system and beyond publication-title: Am. J. Physiol. Heart Circ. Physiol. doi: 10.1152/ajpheart.00373.2017 |
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Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and... Background: Ectopic activation of renin-angiotensin-system contributes to cardiovascular and renal diseases. (Pro)renin receptor (PRR) binds to renin and... |
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| Title | Inhibitory effect of (pro)renin receptor decoy inhibitor PRO20 on endoplasmic reticulum stress during cardiac remodeling |
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