Cardioprotective effects of Ang-(1-7) on the rat myocarditis model

Although it is more common in young people, myocarditis can effect people of all ages, with an incidence of 0.12-12 % due to the variability of its clinical findings. There are two types of etiological factors: infectious and non infectious. Myocarditis has an unclear pathophysiology; it is essentially an inflammatory disease. When myocardial muscle is involved, the cytoskeletal proteins of cardiomyocytes are disrupted, resulting in myocardial damage. DNA damage, mitochondrial dysfunction, oxidative stress, autophagy and metabolic inflammation are all mechanisms of cardiotoxicity caused by the most commonly used anthracycline anticancer agents, such as doxorubicin. Autophagy is a process that aims to provide cell and tissue homeostasis under metabolic stress as well as under normal conditions for nutrient starvation, changes in metabolism, ROS accumulation, energy and oxygen status. This process is aided by proteins and cytosolic components involved in autophagy, which include various subdivisions. Angiotensin (1-7) [ Ang-(1-7) ], an active component of the Renin Angiotensin System (RAS), is produced by the action of angiotensin converting enzyme 2 (ACE2) from Angiotensin II (Ang II). It exerts its action by interacting with the Mas receptor, one of the G protein- coupled receptors found on the cell membrane. Ang-(1-7) has been shown in studies to have vasodilator, anti- inflammatory, antifibrotic and natriuretic properties. The effects of Ang-(1-7) in the rat myocarditis model induced by a single dose of Doxorubucin in heart and serum samples obtained in real time PCR and ELISA studies were investigated in this study. At the conclusion of the study, it was discovered that Ang-(1-7) levels were low in the heart tissues of rats given only Doxorubucin, but high in the serum, whereas ACE2 levels were significantly lower in the heart tissue of the group that only received Doxorubucin. AT1 receptor expression was found to be significantly lower in the Ang-(1-7) treated group. As a result, the Ang-(1-7) myocarditis model in rats exhibits its effect via autophagy-independent mechanisms.