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 the main pathways elicited by their imbalance during age-related muscle wasting. We also discuss lifestyle interventions (i.e., physical exercise and nutrition) that may be exploited to preserve mitochondrial function in the aged muscle. Finally, we illustrate the emerging possibility of rescuing muscle tissue homeostasis through mitochondrial transplantation.