Key result
Angiotensin 1-7 improves ischemia/reperfusion tolerance and mitigates adverse cardiac remodeling via Mas receptor activation.
Why the study?
Mortality among patients with acute myocardial infarction has not significantly decreased over the past decade, creating an urgent need for fundamentally new cardioprotective drugs.
Does angiotensin 1-7 improve cardiac tolerance to ischemia/reperfusion and mitigate adverse remodeling in preclinical models?
Does angiotensin 1-7 improve cardiac tolerance to ischemia/reperfusion and mitigate adverse remodeling in preclinical models?
Angiotensin 1-7 demonstrates cardioprotective properties against ischemia/reperfusion injury in preclinical models, highlighting its potential as a therapeutic target for acute myocardial infarction.
Supports Mas receptor agonism in preclinical ischemia/reperfusion models; leaves open clinical translation to human cardioprotection.
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 Ca 2+ 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.
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Derkachev et al. (2024) conducted a review in Acute myocardial infarction. Angiotensin 1-7 was evaluated. Angiotensin 1-7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart, primarily through Mas receptor activation.
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