Key result
Alamandine acts through the MrgD receptor to exert cardioprotective, anti-hypertrophic, and positive inotropic effects in cardiomyocytes across various preclinical models of cardiac injury.
Why the study?
Following the description of alamandine and its receptor MrgD, characterization of their physiological and pathological functions in the heart has emerged, warranting a review of their cardiomyocyte actions.
The alamandine/MrgD axis is a novel counter-regulatory component of the renin-angiotensin system that exerts cardioprotective, anti-hypertrophic, and positive inotropic effects in preclinical models.
The renin-angiotensin system (RAS) is a classical hormonal system involved in a myriad of cardiovascular functions. This system is composed of many different peptides that act in the heart through different receptors. One of the most important of these peptides is angiotensin II, which in pathological conditions triggers a set of actions that lead to heart failure. On the other hand, another RAS peptide, angiotensin-(1-7) is well known to develop powerful therapeutic effects in many forms of cardiac diseases. In the last decade, two new components of RAS were described, the heptapeptide alamandine and its receptor, the Mas-related G protein-coupled receptor member D (MrgD). Since then, great effort was made to characterize their physiological and pathological function in the heart. In this review, we summarize the latest insights about the actions of alamandine/MrgD axis in the heart, with particular emphasis in the cardiomyocyte. More specifically, we focused on their antihypertrophic and contractility effects, and the related molecular events activated in the cardiomyocyte.
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Jesus et al. (2022) conducted a review in Cardiac hypertrophy and heart failure. Alamandine was evaluated. Alamandine acts through the MrgD receptor to exert cardioprotective, anti-hypertrophic, and positive inotropic effects in cardiomyocytes across various preclinical models of cardiac injury.
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