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Current Drug Research Reviews

Editor-in-Chief

ISSN (Print): 2589-9775
ISSN (Online): 2589-9783

Review Article

Modulation of Angiotensin-II and Angiotensin 1-7 Levels Influences Cardiac Function in Myocardial Ischemia-reperfusion Injury

Author(s): Prabhat Kumar Upadhyay, Navneet Thakur, Vishal Kumar Vishwakarma*, Hridaya Shankar Chaurasiya and Tarique Mahmood Ansari

Volume 17, Issue 1, 2025

Published on: 31 January, 2024

Page: [102 - 112] Pages: 11

DOI: 10.2174/0125899775280160240122065607

Price: $65

Abstract

The angiotensin-converting enzyme-2 (ACE-2) alters the pathophysiology of various fatal cardiovascular diseases, including ischemic heart disease, whereas angiotensin 1-7 (Ang 1–7) exerts a wide range of actions. The effects of ischemia-reperfusion (IR) injury include damage to myocardial tissue that initiates protease action, causing cardiac cell death. Angiotensin- II (Ang-II) contributes through the renin-angiotensin system (RAS) to the IR injury, whereas Ang 1–7 paradoxically exerts a protective effect through the same. Thus, the myocardial ischemic reperfusion injury (MIRI) may be altered by the RAS of the heart. This review paper focuses on ACE-2, angiotensin-converting enzyme (ACE), and Ang 1–7 regulation in the RAS of the heart in the pathophysiology of MIRI. The treatment in such conditions using ACE-2 activator, ACE inhibitor, and Ang-II antagonists may promote vascular functions as well as cardio- protection.

Keywords: Heart, renin-angiotensin system, myocardial ischemia-reperfusion injury, ACE-2 activator, ACE inhibitor, angiotensin-II antagonist.

Graphical Abstract
[1]
Sreeniwas Kumar A, Sinha N. Cardiovascular disease in India: A 360 degree overview. Med J Armed Forces India 2020; 76(1): 1-3.
[http://dx.doi.org/10.1016/j.mjafi.2019.12.005] [PMID: 32020960]
[2]
Nag T, Ghosh A. Cardiovascular disease risk factors in Asian Indian population: A systematic review. J Cardiovasc Dis Res 2013; 4(4): 222-8.
[PMID: 24653585]
[3]
Kontos MC, Diercks DB, Kirk JD. Emergency department and office-based evaluation of patients with chest pain. Mayo Clin Proc 2010; 85(3): 284-99.
[http://dx.doi.org/10.4065/mcp.2009.0560] [PMID: 20194155]
[4]
Goyal A, Agrawal N. Ischemic preconditioning: Interruption of various disorders. J Saudi Heart Assoc 2017; 29(2): 116-27.
[http://dx.doi.org/10.1016/j.jsha.2016.09.002] [PMID: 28373786]
[5]
Ferdinandy P, Hausenloy DJ, Heusch G, Baxter GF, Schulz R. Interaction of risk factors, comorbidities, and comedications with ischemia/reperfusion injury and cardioprotection by preconditioning, postconditioning, and remote conditioning. Pharmacol Rev 2014; 66(4): 1142-74.
[http://dx.doi.org/10.1124/pr.113.008300] [PMID: 25261534]
[6]
Charlson FJ, Moran AE, Freedman G, et al. The contribution of major depression to the global burden of ischemic heart disease: A comparative risk assessment. BMC Med 2013; 11(1): 250.
[http://dx.doi.org/10.1186/1741-7015-11-250] [PMID: 24274053]
[7]
Heusch G, Gersh BJ. The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: A continual challenge. Eur Heart J 2017; 38(11): 774-84.
[PMID: 27354052]
[8]
Philip F, Blackstone E, Kapadia SR. Impact of statins and beta-blocker therapy on mortality after coronary artery bypass graft surgery. Cardiovasc Diagn Ther 2015; 5(1): 8-16.
[PMID: 25774344]
[9]
Gracia-Sancho J, Casillas-Ramírez A, Peralta C. Molecular pathways in protecting the liver from ischaemia/reperfusion injury: A 2015 update. Clin Sci 2015; 129(4): 345-62.
[http://dx.doi.org/10.1042/CS20150223] [PMID: 26014222]
[10]
Jespersen NR, Yokota T, Støttrup NB, et al. Pre‐ischaemic mitochondrial substrate constraint by inhibition of malate‐aspartate shuttle preserves mitochondrial function after ischaemia–reperfusion. J Physiol 2017; 595(12): 3765-80.
[http://dx.doi.org/10.1113/JP273408] [PMID: 28093764]
[11]
Wu MY, Yiang GT, Liao WT, et al. Current mechanistic concepts in ischemia and reperfusion injury. Cell Physiol Biochem 2018; 46(4): 1650-67.
[http://dx.doi.org/10.1159/000489241] [PMID: 29694958]
[12]
Montezano AC, Touyz RM. Molecular mechanisms of hypertension-reactive oxygen species and antioxidants: A basic science update for the clinician. Can J Cardiol 2012; 28(3): 288-95.
[http://dx.doi.org/10.1016/j.cjca.2012.01.017] [PMID: 22445098]
[13]
Sharifi-Rad M, Anil Kumar NV, Zucca P, et al. Lifestyle, oxidative stress, and antioxidants: Back and forth in the pathophysiology of chronic diseases. Front Physiol 2020; 11: 694.
[http://dx.doi.org/10.3389/fphys.2020.00694] [PMID: 32714204]
[14]
Rana AK, Singh D. Targeting glycogen synthase kinase-3 for oxidative stress and neuroinflammation: Opportunities, challenges and future directions for cerebral stroke management. Neuropharmacology 2018; 139: 124-36.
[http://dx.doi.org/10.1016/j.neuropharm.2018.07.006] [PMID: 30017999]
[15]
Lamendola P, Di Monaco A, Barone L, Pisanello C, Lanza GA, Crea F. Mechanisms of myocardial cell protection from ischemia/reperfusion injury and potential clinical implications. G Ital Cardiol 2009; 10(1): 28-36.
[PMID: 19292017]
[16]
Petrosillo G, Di Venosa N, Moro N, et al. In vivo hyperoxic preconditioning protects against rat-heart ischemia/reperfusion injury by inhibiting mitochondrial permeability transition pore opening and cytochrome c release. Free Radic Biol Med 2011; 50(3): 477-83.
[http://dx.doi.org/10.1016/j.freeradbiomed.2010.11.030] [PMID: 21130864]
[17]
Baines CP. The mitochondrial permeability transition pore and ischemia-reperfusion injury. Basic Res Cardiol 2009; 104(2): 181-8.
[http://dx.doi.org/10.1007/s00395-009-0004-8] [PMID: 19242640]
[18]
Brentnall M, Rodriguez-Menocal L, De Guevara RL, Cepero E, Boise LH. Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis. BMC Cell Biol 2013; 14(1): 32.
[http://dx.doi.org/10.1186/1471-2121-14-32] [PMID: 23834359]
[19]
Brentnall M, Weir DB, Rongvaux A, Marcus AI, Boise LH. Procaspase-3 regulates fibronectin secretion and influences adhesion, migration and survival independently of catalytic function. J Cell Sci 2014; 127(Pt 10): 2217-26.
[PMID: 24610949]
[20]
Messner B, Türkcan A, Ploner C, Laufer G, Bernhard D. Cadmium overkill: Autophagy, apoptosis and necrosis signalling in endothelial cells exposed to cadmium. Cell Mol Life Sci 2016; 73(8): 1699-713.
[http://dx.doi.org/10.1007/s00018-015-2094-9] [PMID: 26588916]
[21]
Cadenas S. ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection. Free Radic Biol Med 2018; 117: 76-89.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.01.024] [PMID: 29373843]
[22]
Houang EM, Bartos J, Hackel BJ, et al. Cardiac muscle membrane stabilization in myocardial reperfusion injury. JACC Basic Transl Sci 2019; 4(2): 275-87.
[http://dx.doi.org/10.1016/j.jacbts.2019.01.009] [PMID: 31061929]
[23]
Bagheri F, Khori V, Alizadeh AM, Khalighfard S, Khodayari S, Khodayari H. Reactive oxygen species-mediated cardiac-reperfusion injury: Mechanisms and therapies. Life Sci 2016; 165: 43-55.
[http://dx.doi.org/10.1016/j.lfs.2016.09.013] [PMID: 27667751]
[24]
Zheng Y, Xu L, Dong N, Li F. NLRP3 inflammasome: The rising star in cardiovascular diseases. Front Cardiovasc Med 2022; 9: 927061.
[http://dx.doi.org/10.3389/fcvm.2022.927061] [PMID: 36204568]
[25]
Miura T, Tanno M. Mitochondria and GSK-3beta in cardioprotection against ischemia/reperfusion injury. Cardiovasc Drugs Ther 2010; 24(3): 255-63.
[http://dx.doi.org/10.1007/s10557-010-6234-z] [PMID: 20490903]
[26]
Halestrap AP. Calcium, mitochondria and reperfusion injury: A pore way to die. Biochem Soc Trans 2006; 34(2): 232-7.
[http://dx.doi.org/10.1042/BST0340232] [PMID: 16545083]
[27]
Thirupathi A, Pinho RA. Effects of reactive oxygen species and interplay of antioxidants during physical exercise in skeletal muscles. J Physiol Biochem 2018; 74(3): 359-67.
[http://dx.doi.org/10.1007/s13105-018-0633-1] [PMID: 29713940]
[28]
Neri M, Riezzo I, Pascale N, Pomara C, Turillazzi E. Ischemia/reperfusion injury following acute myocardial infarction: A critical issue for clinicians and forensic pathologists. Mediators Inflamm 2017; 2017: 1-14.
[http://dx.doi.org/10.1155/2017/7018393] [PMID: 28286377]
[29]
Avtaar Singh SS, Das De S, Al-Adhami A, Singh R, Hopkins PMA, Curry PA. Primary graft dysfunction following lung transplantation: From pathogenesis to future frontiers. World J Transplant 2023; 13(3): 58-85.
[http://dx.doi.org/10.5500/wjt.v13.i3.58] [PMID: 36968136]
[30]
Herrington CS, Prekker ME, Arrington AK, et al. A randomized, placebo-controlled trial of aprotinin to reduce primary graft dysfunction following lung transplantation. Clin Transplant 2011; 25(1): 90-6.
[http://dx.doi.org/10.1111/j.1399-0012.2010.01319.x] [PMID: 20731686]
[31]
Granger DN, Kvietys PR. Reperfusion injury and reactive oxygen species: The evolution of a concept. Redox Biol 2015; 6: 524-51.
[http://dx.doi.org/10.1016/j.redox.2015.08.020] [PMID: 26484802]
[32]
Kotyla P. Bimodal function of anti-TNF treatment: Shall we be concerned about anti-tnf treatment in patients with rheumatoid arthritis and heart failure? Int J Mol Sci 2018; 19(6): 1739.
[http://dx.doi.org/10.3390/ijms19061739] [PMID: 29895751]
[33]
Paravicini TM, Touyz RM. NADPH oxidases, reactive oxygen species, and hypertension: Clinical implications and therapeutic possibilities. Diabetes Care 2008; 31 (Suppl. 2): S170-80.
[http://dx.doi.org/10.2337/dc08-s247] [PMID: 18227481]
[34]
Malek M, Nematbakhsh M. Renal ischemia/reperfusion injury: From pathophysiology to treatment. J Renal Inj Prev 2015; 4(2): 20-7.
[PMID: 26060833]
[35]
Jang HR, Rabb H. The innate immune response in ischemic acute kidney injury. Clin Immunol 2009; 130(1): 41-50.
[http://dx.doi.org/10.1016/j.clim.2008.08.016] [PMID: 18922742]
[36]
Sharfuddin AA, Molitoris BA. Pathophysiology of ischemic acute kidney injury. Nat Rev Nephrol 2011; 7(4): 189-200.
[http://dx.doi.org/10.1038/nrneph.2011.16] [PMID: 21364518]
[37]
de Groot H, Rauen U. Ischemia-reperfusion injury: Processes in pathogenetic networks: A review. Transplant Proc 2007; 39(2): 481-4.
[http://dx.doi.org/10.1016/j.transproceed.2006.12.012] [PMID: 17362763]
[38]
Khurana S, Venkataraman K, Hollingsworth A, Piche M, Tai T. Polyphenols: Benefits to the cardiovascular system in health and in aging. Nutrients 2013; 5(10): 3779-827.
[http://dx.doi.org/10.3390/nu5103779] [PMID: 24077237]
[39]
Yu H, Kalogeris T, Korthuis RJ. Reactive species-induced microvascular dysfunction in ischemia/reperfusion. Free Radic Biol Med 2019; 135: 182-97.
[http://dx.doi.org/10.1016/j.freeradbiomed.2019.02.031] [PMID: 30849489]
[40]
Ajmani P, Yadav HN, Singh M, Sharma PL. Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart. BMC Cardiovasc Disord 2011; 11(1): 43.
[http://dx.doi.org/10.1186/1471-2261-11-43] [PMID: 21745415]
[41]
Gupta I, Goyal A, Singh NK, Yadav HN, Sharma PL. Hemin, a heme oxygenase-1 inducer, restores the attenuated cardioprotective effect of ischemic preconditioning in isolated diabetic rat heart. Hum Exp Toxicol 2017; 36(8): 867-75.
[http://dx.doi.org/10.1177/0960327116673169] [PMID: 27738197]
[42]
Heusch G. Myocardial ischaemia–reperfusion injury and cardioprotection in perspective. Nat Rev Cardiol 2020; 17(12): 773-89.
[http://dx.doi.org/10.1038/s41569-020-0403-y] [PMID: 32620851]
[43]
Hausenloy DJ, Botker HE, Engstrom T, et al. Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: Trials and tribulations. Eur Heart J 2017; 38(13): 935-41.
[PMID: 27118196]
[44]
Minasian SM, Galagudza MM, Dmitriev YV, Karpov AA, Vlasov TD. Preservation of the donor heart: From basic science to clinical studies. Interact Cardiovasc Thorac Surg 2015; 20(4): 510-9.
[http://dx.doi.org/10.1093/icvts/ivu432] [PMID: 25538253]
[45]
Jonecova Z, Toth S, Maretta M, et al. Protective effect of ischemic preconditioning on the jejunal graft mucosa injury during cold preservation. Exp Mol Pathol 2015; 99(2): 229-35.
[http://dx.doi.org/10.1016/j.yexmp.2015.06.020] [PMID: 26123930]
[46]
Pagliaro P, Penna C. Rethinking the renin-angiotensin system and its role in cardiovascular regulation. Cardiovasc Drugs Ther 2005; 19(1): 77-87.
[http://dx.doi.org/10.1007/s10557-005-6900-8] [PMID: 15883759]
[47]
Penna C, Tullio F, Moro F, Folino A, Merlino A, Pagliaro P. Effects of a protocol of ischemic postconditioning and/or captopril in hearts of normotensive and hypertensive rats. Basic Res Cardiol 2010; 105(2): 181-92.
[http://dx.doi.org/10.1007/s00395-009-0075-6] [PMID: 20012872]
[48]
Ferdinandy P, Andreadou I, Baxter GF, et al. Interaction of cardiovascular nonmodifiable risk factors, comorbidities and comedications with ischemia/reperfusion injury and cardioprotection by pharmacological treatments and ischemic conditioning. Pharmacol Rev 2023; 75(1): 159-216.
[http://dx.doi.org/10.1124/pharmrev.121.000348] [PMID: 36753049]
[49]
Nankivell BJ, Kuypers DRJ. Diagnosis and prevention of chronic kidney allograft loss. Lancet 2011; 378(9800): 1428-37.
[http://dx.doi.org/10.1016/S0140-6736(11)60699-5] [PMID: 22000139]
[50]
Randhawa PK, Bali A, Jaggi AS. RIPC for multiorgan salvage in clinical settings: Evolution of concept, evidences and mechanisms. Eur J Pharmacol 2015; 746: 317-32.
[http://dx.doi.org/10.1016/j.ejphar.2014.08.016] [PMID: 25176179]
[51]
Püchel J, Sitter M, Kranke P, Pecks U. Procedural techniques to control postpartum hemorrhage. Baillieres Best Pract Res Clin Anaesthesiol 2022; 36(3-4): 371-82.
[http://dx.doi.org/10.1016/j.bpa.2022.09.002] [PMID: 36513432]
[52]
Guo L, Sun G, Wang G, Ning W, Zhao K. Soluble P-selectin promotes acute myocardial infarction onset but not severity. Mol Med Rep 2015; 11(3): 2027-33.
[http://dx.doi.org/10.3892/mmr.2014.2917] [PMID: 25384966]
[53]
Weil BR, Neelamegham S. Selectins and immune cells in acute myocardial infarction and post-infarction ventricular remodeling: Pathophysiology and novel treatments. Front Immunol 2019; 10: 300.
[http://dx.doi.org/10.3389/fimmu.2019.00300] [PMID: 30873166]
[54]
Oh KS, Seo HW, Yi KY, Lee S, Yoo S, Lee BH. Effects of KR‐33028, a novel Na +/H + exchanger‐1 inhibitor, on ischemia and reperfusion‐induced myocardial infarction in rats and dogs. Fundam Clin Pharmacol 2007; 21(3): 255-63.
[http://dx.doi.org/10.1111/j.1472-8206.2007.00491.x] [PMID: 17521294]
[55]
Simões e Silva AC, Teixeira MM. ACE inhibition, ACE2 and angiotensin-(1⿿7) axis in kidney and cardiac inflammation and fibrosis. Pharmacol Res 2016; 107: 154-62.
[http://dx.doi.org/10.1016/j.phrs.2016.03.018] [PMID: 26995300]
[56]
Lima CT, Silva JCS, Viegas KAS, et al. Increase in vascular injury of sodium overloaded mice may be related to vascular angiotensin modulation. PLoS One 2015; 10(6): e0128141.
[http://dx.doi.org/10.1371/journal.pone.0128141] [PMID: 26030299]
[57]
De Resende MM, Mill JG. Effect of high salt intake on local renin-angiotensin system and ventricular dysfunction following myocardial infarction in rats. Clin Exp Pharmacol Physiol 2007; 34(4): 274-9.
[http://dx.doi.org/10.1111/j.1440-1681.2007.04556.x] [PMID: 17324137]
[58]
Paul M, Poyan Mehr A, Kreutz R. Physiology of local renin-angiotensin systems. Physiol Rev 2006; 86(3): 747-803.
[http://dx.doi.org/10.1152/physrev.00036.2005] [PMID: 16816138]
[59]
Iwata M, Cowling RT, Yeo SJ, Greenberg B. Targeting the ACE2–Ang-(1–7) pathway in cardiac fibroblasts to treat cardiac remodeling and heart failure. J Mol Cell Cardiol 2011; 51(4): 542-7.
[http://dx.doi.org/10.1016/j.yjmcc.2010.12.003] [PMID: 21147120]
[60]
Hamming I, Timens W, Bulthuis MLC, Lely AT, Navis GJ, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 2004; 203(2): 631-7.
[http://dx.doi.org/10.1002/path.1570] [PMID: 15141377]
[61]
Shi L, Mao C, Xu Z, Zhang L. Angiotensin-converting enzymes and drug discovery in cardiovascular diseases. Drug Discov Today 2010; 15(9-10): 332-41.
[http://dx.doi.org/10.1016/j.drudis.2010.02.003] [PMID: 20170743]
[62]
Ryu WS, Kim SW, Kim CJ. Overview of the renin-angiotensin system. Korean Circ J 2007; 37(3): 91-6.
[http://dx.doi.org/10.4070/kcj.2007.37.3.91]
[63]
Hayden MR, Sowers KM, Pulakat L, et al. Possible mechanisms of local tissue renin-angiotensin system activation in the cardiorenal metabolic syndrome and type 2 diabetes mellitus. Cardiorenal Med 2011; 1(3): 193-210.
[http://dx.doi.org/10.1159/000329926] [PMID: 22096455]
[64]
Sabharwal R, Chapleau MW. Autonomic, locomotor and cardiac abnormalities in a mouse model of muscular dystrophy: Targeting the renin–angiotensin system. Exp Physiol 2014; 99(4): 627-31.
[http://dx.doi.org/10.1113/expphysiol.2013.074336] [PMID: 24334334]
[65]
Gutte H, Oxbøl J, Kristoffersen US, Mortensen J, Kjær A. Gene expression of ANP, BNP and ET-1 in the heart of rats during pulmonary embolism. PLoS One 2010; 5(6): e11111.
[http://dx.doi.org/10.1371/journal.pone.0011111] [PMID: 20559433]
[66]
Marangoni RA, Santos RA, Piccolo C. Deficient prolylcarboxypeptidase gene and protein expression in left ventricles of spontaneously hypertensive rats (SHR). Peptides 2014; 61: 69-74.
[http://dx.doi.org/10.1016/j.peptides.2014.08.016] [PMID: 25218829]
[67]
Sparks MA, Crowley SD, Gurley SB, Mirotsou M, Coffman TM. Classical renin-angiotensin system in kidney physiology. Compr Physiol 2014; 4(3): 1201-28.
[http://dx.doi.org/10.1002/cphy.c130040] [PMID: 24944035]
[68]
Gonsalez SR, Ferrão FM, Souza AM, Lowe J, Morcillo LSL. Inappropriate activity of local renin-angiotensin-aldosterone system during high salt intake: Impact on the cardio-renal axis. J Bras Nefrol 2018; 40(2): 170-8.
[http://dx.doi.org/10.1590/2175-8239-jbn-3661] [PMID: 29944159]
[69]
Husková Z, Kopkan L, Červenková L, et al. Intrarenal alterations of the angiotensin‐converting enzyme type 2/angiotensin 1–7 complex of the renin‐angiotensin system do not alter the course of malignant hypertension in Cyp1a1‐Ren‐2 transgenic rats. Clin Exp Pharmacol Physiol 2016; 43(4): 438-49.
[http://dx.doi.org/10.1111/1440-1681.12553] [PMID: 26833491]
[70]
Satou R, Gonzalez-Villalobos RA. JAK-STAT and the renin-angiotensin system. JAK-STAT 2012; 1(4): 250-6.
[http://dx.doi.org/10.4161/jkst.22729] [PMID: 24058780]
[71]
Roshanov PS, Rochwerg B, Patel A, et al. Withholding versus continuing angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers before noncardiac surgery: An analysis of the vascular events in noncardiac surgery patients cohort evaluation prospective cohort. Anesthesiology 2017; 126(1): 16-27.
[http://dx.doi.org/10.1097/ALN.0000000000001404] [PMID: 27775997]
[72]
Min LJ, Mogi M, Li JM, Iwanami J, Iwai M, Horiuchi M. Aldosterone and angiotensin II synergistically induce mitogenic response in vascular smooth muscle cells. Circ Res 2005; 97(5): 434-42.
[http://dx.doi.org/10.1161/01.RES.0000180753.63183.95] [PMID: 16081869]
[73]
Zhang Y, Griendling KK, Dikalova A, Owens GK, Taylor WR. Vascular hypertrophy in angiotensin II-induced hypertension is mediated by vascular smooth muscle cell-derived H2O2. Hypertension 2005; 46(4): 732-7.
[http://dx.doi.org/10.1161/01.HYP.0000182660.74266.6d] [PMID: 16172434]
[74]
Ushio-Fukai M, Zuo L, Ikeda S, Tojo T, Patrushev NA, Alexander RW. cAbl tyrosine kinase mediates reactive oxygen species- and caveolin-dependent AT1 receptor signaling in vascular smooth muscle: role in vascular hypertrophy. Circ Res 2005; 97(8): 829-36.
[http://dx.doi.org/10.1161/01.RES.0000185322.46009.F5] [PMID: 16151024]
[75]
Warner FJ, Lew RA, Smith AI, Lambert DW, Hooper NM, Turner AJ. Angiotensin-converting enzyme 2 (ACE2), but not ACE, is preferentially localized to the apical surface of polarized kidney cells. J Biol Chem 2005; 280(47): 39353-62.
[http://dx.doi.org/10.1074/jbc.M508914200] [PMID: 16166094]
[76]
Jiang T, Gao L, Lu J, Zhang YD. ACE2-Ang-(1-7)-Mas axis in brain: A potential target for prevention and treatment of ischemic stroke. Curr Neuropharmacol 2013; 11(2): 209-17.
[http://dx.doi.org/10.2174/1570159X11311020007] [PMID: 23997755]
[77]
Samavati L, Uhal BD. ACE2, much more than just a receptor for SARS-COV-2. Front Cell Infect Microbiol 2020; 10: 317.
[http://dx.doi.org/10.3389/fcimb.2020.00317] [PMID: 32582574]
[78]
Gheblawi M, Wang K, Viveiros A, et al. Angiotensin-converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system. Circ Res 2020; 126(10): 1456-74.
[http://dx.doi.org/10.1161/CIRCRESAHA.120.317015] [PMID: 32264791]
[79]
Forrester SJ, Booz GW, Sigmund CD, et al. Angiotensin II signal transduction: An update on mechanisms of physiology and pathophysiology. Physiol Rev 2018; 98(3): 1627-738.
[http://dx.doi.org/10.1152/physrev.00038.2017] [PMID: 29873596]
[80]
Solomon SD, Pfeffer MA. The decreasing incidence of left ventricular remodeling following myocardial infarction. Basic Res Cardiol 1997; 92(2): 61-5.
[http://dx.doi.org/10.1007/BF00805561] [PMID: 9166980]
[81]
Zhang T, Ma C, Zhang Z, Zhang H, Hu H. NF‐κB signaling in inflammation and cancer. MedComm 2021; 2(4): 618-53.
[http://dx.doi.org/10.1002/mco2.104] [PMID: 34977871]
[82]
Ehring T, Baumgart D, Krajcar M, Hümmelgen M, Kompa S, Heusch G. Attenuation of myocardial stunning by the ACE inhibitor ramiprilat through a signal cascade of bradykinin and prostaglandins but not nitric oxide. Circulation 1994; 90(3): 1368-85.
[http://dx.doi.org/10.1161/01.CIR.90.3.1368] [PMID: 8087948]
[83]
Frangogiannis NG. Transforming growth factor–β in tissue fibrosis. J Exp Med 2020; 217(3): e20190103.
[http://dx.doi.org/10.1084/jem.20190103] [PMID: 32997468]
[84]
Sousa-Lopes A, de Freitas RA, Carneiro FS, et al. Angiotensin (1-7) inhibits Ang II-mediated ERK1/2 activation by stimulating MKP-1 activation in vascular smooth muscle cells. Int J Mol Cell Med 2020; 9(1): 50-61.
[PMID: 32832484]
[85]
Jalowy A, Schulz R, Dörge H, Behrends M, Heusch G. Infarct size reduction by AT1-receptor blockade through a signal cascade of AT2-receptor activation, bradykinin and prostaglandins in pigs. J Am Coll Cardiol 1998; 32(6): 1787-96.
[http://dx.doi.org/10.1016/S0735-1097(98)00441-0] [PMID: 9822110]
[86]
Dörge H, Behrends M, Schulz R, Jalowy A, Heusch G. Attenuation of myocardial stunning by the AT 1 receptor antagonist candesartan. Basic Res Cardiol 1999; 94(3): 208-14.
[http://dx.doi.org/10.1007/s003950050144] [PMID: 10424239]
[87]
AlQudah M, Hale TM, Czubryt MP. Targeting the renin-angiotensin-aldosterone system in fibrosis. Matrix Biol 2020; 91-92: 92-108.
[http://dx.doi.org/10.1016/j.matbio.2020.04.005] [PMID: 32422329]
[88]
Ong SB, Hernández-Reséndiz S, Crespo-Avilan GE, et al. Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacol Ther 2018; 186: 73-87.
[http://dx.doi.org/10.1016/j.pharmthera.2018.01.001] [PMID: 29330085]
[89]
Babiker F, Al-Jarallah A, Joseph S. The interplay between the renin angiotensin system and pacing postconditioning induced cardiac protection. PLoS One 2016; 11(11): e0165777.
[http://dx.doi.org/10.1371/journal.pone.0165777] [PMID: 27814397]
[90]
Meier P, Maillard M, Burnier M. The future of angiotensin II inhibition in cardiovascular medicine. Curr Drug Targets Cardiovasc Haematol Disord 2005; 5(1): 15-30.
[http://dx.doi.org/10.2174/1568006053004994] [PMID: 15720221]
[91]
Qi Y, Zhang J, Cole-Jeffrey CT, et al. Diminazene aceturate enhances angiotensin-converting enzyme 2 activity and attenuates ischemia-induced cardiac pathophysiology. Hypertension 2013; 62(4): 746-52.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.113.01337] [PMID: 23959549]
[92]
Castardeli C, Sartório CL, Pimentel EB, Forechi L, Mill JG. The ACE 2 activator diminazene aceturate (DIZE) improves left ventricular diastolic dysfunction following myocardial infarction in rats. Biomed Pharmacother 2018; 107: 212-8.
[http://dx.doi.org/10.1016/j.biopha.2018.07.170] [PMID: 30092400]
[93]
Martínez LA, Villalobos-Molina R. Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats. Arch Med Res 2003; 34(5): 357-61.
[http://dx.doi.org/10.1016/S0188-4409(03)00076-6] [PMID: 14602500]
[94]
Pagliaro P, Penna C. ACE/ACE2 ratio: A key also in 2019 coronavirus disease (Covid-19)? Front Med 2020; 7: 335.
[http://dx.doi.org/10.3389/fmed.2020.00335] [PMID: 32626721]
[95]
Huang J, Tang X, Liang X, et al. The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on pressure overload-induced cardiac remodeling in rats and the endothelial mechanisms based on PGI2. Cell Physiol Biochem 2015; 36(3): 1004-14.
[http://dx.doi.org/10.1159/000430274] [PMID: 26112123]
[96]
Xue B, Zhang Y, Johnson AK. Interactions of the brain renin-angiotensin-system (RAS) and inflammation in the sensitization of hypertension. Front Neurosci 2020; 14: 650.
[http://dx.doi.org/10.3389/fnins.2020.00650] [PMID: 32760236]
[97]
Busse LW, Chow JH, McCurdy MT, Khanna AK. COVID-19 and the RAAS—a potential role for angiotensin II? Crit Care 2020; 24(1): 136.
[http://dx.doi.org/10.1186/s13054-020-02862-1] [PMID: 32264922]
[98]
Singh AK, Gupta R, Misra A. Comorbidities in COVID-19: Outcomes in hypertensive cohort and controversies with renin angiotensin system blockers. Diabetes Metab Syndr 2020; 14(4): 283-7.
[http://dx.doi.org/10.1016/j.dsx.2020.03.016] [PMID: 32283499]
[99]
Penna C, Mercurio V, Tocchetti CG, Pagliaro P. Sex‐related differences in COVID‐19 lethality. Br J Pharmacol 2020; 177(19): 4375-85.
[http://dx.doi.org/10.1111/bph.15207] [PMID: 32698249]
[100]
Ciaglia E, Vecchione C, Puca AA. COVID-19 infection and circulating ACE2 levels: Protective role in women and children. Front Pediatr 2020; 8: 206.
[http://dx.doi.org/10.3389/fped.2020.00206] [PMID: 32391299]

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