Angiotensin-(1–7) decreases skeletal muscle atrophy induced by angiotensin II through a Mas receptor-dependent mechanism

摘要: Skeletal muscle atrophy is a pathological condition characterized by the loss of strength and mass, an increase in myosin heavy chain (MHC) degradation expression two muscle-specific ubiquitin ligases: atrogin-1 MuRF-1. Angiotensin II (AngII) induces atrophy. Angiotensin-(1-7) [Ang-(1-7)], through its receptor Mas, produces opposite effects than AngII. We assessed Ang-(1-7) on skeletal induced Our results show that Ang-(1-7), prevents AngII gastrocnemius: decrease fibre diameter, MHC levels also AKT phosphorylation. In addition, our analysis vitro using C2C12 myotubes shows mechanism dependent MuRF-1, both phosphorylation myotubes; additionally, we demonstrated inhibition with MK-2206 decreases anti-atrophic Ang-(1-7). Thus, demonstrate for first time counteracts Mas receptor, which involves activity. study indicates novel molecule potential therapeutical use to improve wasting associated, at least, pathologies present high