Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.

BACKGROUND

Sarcopenia is a degenerative muscular disease associated with aging, characterized by a reduction in muscle mass and strength. This disease poses a significant global health challenge, owing to its high prevalence and association with adverse outcomes such as increased frailty, impaired physical function, and elevated mortality risk. A deeper understanding of its underlying mechanisms is urgently warranted for the development of effective therapeutic interventions.

AIM OF REVIEW: Skeletal muscle is a heterogeneous tissue composed of various cellular components, including myofibers and other muscle-resident cells such as satellite cells, neurons and immune cells. Myofibers serve as the fundamental units determining muscle mass and strength, while muscle-resident cells establish the skeletal muscle microenvironment (SMME), which plays a significant role in maintaining skeletal muscle health. This review aimed to systematically dissect the crosstalk between myofibers and the SMME, and develop potential therapeutic interventions by highlighting novel insights into the pathogenesis of sarcopenia.

KEY SCIENTIFIC CONCEPTS OF REVIEW: This review provides a comprehensive overview of the age-related changes in various SMME components, with a specific focus on the disrupted interactions between them and myofibers during aging.