Why the study?
Myocardial ischemia-reperfusion injury may be altered by the cardiac renin-angiotensin system, where Ang-II contributes to injury while Ang 1-7 exerts protective effects.
Modulation of the renin-angiotensin system, specifically through ACE-2, ACE, and Ang 1-7, plays a crucial role in the pathophysiology and potential treatment of myocardial ischemia-reperfusion injury.
Ang 1-7 may protect against IR injury; leaves open clinical translation of ACE-2/Ang 1-7 modulation.
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.
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Upadhyay et al. (2024) studied this question.
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