Mitochondrial Quantity and Quality in Age-Related Sarcopenia

first_page settings Order Article Reprints Open AccessReview Mitochondrial Quantity and Quality in Age-Related Sarcopenia by Emanuele Marzetti 1,2,* [ORCID] , Riccardo Calvani 1,2 [ORCID] , Hélio José Coelho-Júnior 2 [ORCID] , Francesco Landi 1,2 and Anna Picca 1,3,* [ORCID] 1 Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS, L.go A. Gemelli 8, 00168 Rome, Italy 2 Department of Geriatrics, Orthopedics and Rheumatology, Università Cattolica del Sacro Cuore, L.go F. Vito 1, 00618 Rome, Italy 3 Department of Medicine and Surgery, LUM University, SS100 km 18, 70010 Casamassima, Italy * Authors to whom correspondence should be addressed. Int. J. Mol. Sci. 2024, 25(4), 2052; https://doi.org/10.3390/ijms25042052 Submission received: 19 December 2023 / Revised: 1 February 2024 / Accepted: 6 February 2024 / Published: 8 February 2024 (This article belongs to the Special Issue A Commemorative Issue in Honour of Rudolf Virchow: From Cell Morphology to Molecular Pathology-Volume 2) Download keyboard_arrow_down Browse Figures Versions Notes Abstract Sarcopenia, the age-associated decline in skeletal muscle mass and strength, is a condition with a complex pathophysiology. Among the factors underlying the development of sarcopenia are the progressive demise of motor neurons, the transition from fast to slow myosin isoform (type II to type I fiber switch), and the decrease in satellite cell number and function. Mitochondrial dysfunction has been indicated as a key contributor to skeletal myocyte decline and loss of physical performance with aging. Several systems have been implicated in the regulation of muscle plasticity and trophism such as the fine-tuned and complex regulation between the stimulator of protein synthesis, mechanistic target of rapamycin (mTOR), and the inhibitor of mTOR, AMP-activated protein kinase (AMPK), that promotes muscle catabolism. Here, we provide an overview of the molecular mechanisms linking mitochondrial signaling and quality with muscle homeostasis and performance and discuss ...