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Endothelin-1 induces cellular senescence and fibrosis in cultured myoblasts. A potential mechanism of aging-related sarcopenia

Elena Alcalde‐Estévez, Ana Asenjo‐Bueno, Patricia Sosa, Gemma Olmos, Patricia Plaza, María Ángeles Caballero Mora, Diego Rodrı́guez-Puyol, María Piedad Ruiz‐Torres, Susana López‐Ongil

2020Aging34 citationsDOIOpen Access PDF

Abstract

relevance of these results, circulating ET-1, muscular strength, muscular fibrosis and p16 expression were measured in male C57Bl6 mice from 5-18-24-months-old. Old mice shown high levels of ET-1 correlated with muscular fibrosis, muscular p16 expression and loss of muscle strength. In conclusion, ET-1 promotes fibrosis and senescence in cultured myoblasts, similar results were found in old mice, suggesting a potential role for ET-1 in the development of sarcopenia related to aging.

Topics & Concepts

SenescenceSarcopeniaFibrosisMyocyteEndothelin 1EndocrinologyInternal medicineMedicineBiologyReceptorTelomeres, Telomerase, and SenescenceMuscle Physiology and DisordersNeutrophil, Myeloperoxidase and Oxidative Mechanisms
Endothelin-1 induces cellular senescence and fibrosis in cultured myoblasts. A potential mechanism of aging-related sarcopenia | Litcius