Skeletal muscle wasting: new role of nonclassical renin–angiotensin system

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Abstract

Purpose of review

Skeletal muscle can be affected by many physiological and pathological conditions that contribute to the development of muscle weakness, including skeletal muscle loss, inflammatory processes, or fibrosis. Therefore, research into therapeutic treatment alternatives or alleviation of these effects on skeletal muscle is of great importance.

Recent findings

Recent studies have shown that angiotensin (1–7) [Ang-(1–7)] – a vasoactive peptide of the nonclassical axis in the renin–angiotensin system (RAS) – and its Mas receptor are expressed in skeletal muscle. Ang-(1–7), through its Mas receptor, prevents or diminishes deleterious effects induced by skeletal muscle disease or injury. Specifically, the Ang-(1–7)–Mas receptor axis modulates molecular mechanisms involved in muscle mass regulation, such as the ubiquitin proteasome pathway, the insulin-like growth factor type 1/Akt (protein kinase B) pathway, or myonuclear apoptosis, and also inflammation and fibrosis pathways.

Summary

Although further research into this topic and the possible side effects of Ang-(1–7) is necessary, these findings are promising, and suggest that the Ang-(1–7)–Mas axis can be considered a possible therapeutic target for treating patients with muscular disorders.

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