Angiotensin 1–7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart—The signaling mechanism

IF 2.1 4区医学 Q3 PHARMACOLOGY & PHARMACY

Fundamental & Clinical Pharmacology Pub Date : 2024-02-04 DOI:10.1111/fcp.12983

Ivan A. Derkachev, Sergey V. Popov, Leonid N. Maslov, Alexandr V. Mukhomedzyanov, Natalia V. Naryzhnaya, Alexander S. Gorbunov, Artur Kan, Andrey V. Krylatov, Yuri K. Podoksenov, Ivan V. Stepanov, Svetlana V. Gusakova, Feng Fu, Jian-Ming Pei

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引用次数: 0

Abstract

Background

The high mortality rate of patients with acute myocardial infarction (AMI) remains the most pressing issue of modern cardiology. Over the past 10 years, there has been no significant reduction in mortality among patients with AMI. It is quite obvious that there is an urgent need to develop fundamentally new drugs for the treatment of AMI. Angiotensin 1–7 has some promise in this regard.

Objective

The objective of this article is analysis of published data on the cardioprotective properties of angiotensin 1–7.

Methods

PubMed, Scopus, Science Direct, and Google Scholar were used to search articles for this study.

Results

Angiotensin 1–7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart. Angiotensin 1–7 can prevent not only ischemic but also reperfusion cardiac injury. The activation of the Mas receptor plays a key role in these effects of angiotensin 1–7. Angiotensin 1–7 alleviates Ca²⁺ overload of cardiomyocytes and reactive oxygen species production in ischemia/reperfusion (I/R) of the myocardium. It is possible that both effects are involved in angiotensin 1–7-triggered cardiac tolerance to I/R. Furthermore, angiotensin 1–7 inhibits apoptosis of cardiomyocytes and stimulates autophagy of cells. There is also indirect evidence suggesting that angiotensin 1–7 inhibits ferroptosis in cardiomyocytes. Moreover, angiotensin 1–7 possesses anti-inflammatory properties, possibly achieved through NF-kB activity inhibition. Phosphoinositide 3-kinase, Akt, and NO synthase are involved in the infarct-reducing effect of angiotensin 1–7. However, the specific end-effector of the cardioprotective impact of angiotensin 1–7 remains unknown.

Conclusion

The molecular nature of the end-effector of the infarct-limiting effect of angiotensin 1–7 has not been elucidated. Perhaps, this end-effector is the sarcolemmal K_ATP channel or the mitochondrial K_ATP channel.

查看原文本刊更多论文

血管紧张素 1-7 增加心脏对缺血/再灌注的耐受性并减轻心脏的不良重塑--信号机制

急性心肌梗死（AMI）患者的高死亡率仍然是现代心脏病学最紧迫的问题。在过去 10 年中，急性心肌梗死患者的死亡率一直没有显著下降。显而易见，治疗急性心肌梗死急需开发全新的药物。在这方面，血管紧张素 1-7 具有一定的前景。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Fundamental & Clinical Pharmacology 医学-药学

CiteScore

5.30

自引率

6.90%

发文量

111

审稿时长

6-12 weeks

期刊介绍： Fundamental & Clinical Pharmacology publishes reports describing important and novel developments in fundamental as well as clinical research relevant to drug therapy. Original articles, short communications and reviews are published on all aspects of experimental and clinical pharmacology including: Antimicrobial, Antiviral Agents Autonomic Pharmacology Cardiovascular Pharmacology Cellular Pharmacology Clinical Trials Endocrinopharmacology Gene Therapy Inflammation, Immunopharmacology Lipids, Atherosclerosis Liver and G-I Tract Pharmacology Metabolism, Pharmacokinetics Neuropharmacology Neuropsychopharmacology Oncopharmacology Pediatric Pharmacology Development Pharmacoeconomics Pharmacoepidemiology Pharmacogenetics, Pharmacogenomics Pharmacovigilance Pulmonary Pharmacology Receptors, Signal Transduction Renal Pharmacology Thrombosis and Hemostasis Toxicopharmacology Clinical research, including clinical studies and clinical trials, may cover disciplines such as pharmacokinetics, pharmacodynamics, pharmacovigilance, pharmacoepidemiology, pharmacogenomics and pharmacoeconomics. Basic research articles from fields such as physiology and molecular biology which contribute to an understanding of drug therapy are also welcomed.