Ontology highlight
ABSTRACT: Introduction
Physical inactivity significantly contributes to loss of muscle mass and performance in bed-bound patients. Loss of skeletal muscle mitochondrial content has been well-established in muscle unloading models, but the underlying molecular mechanism remains unclear. We hypothesized that apparent unloading-induced loss of muscle mitochondrial content is preceded by increased mitophagy- and decreased mitochondrial biogenesis-signaling during the early stages of unloading.Methods
We analyzed a comprehensive set of molecular markers involved in mitochondrial-autophagy, -biogenesis, -dynamics, and -content, in the gastrocnemius muscle of C57BL/6J mice subjected to 0- and 3-days hind limb suspension, and in biopsies from human vastus lateralis muscle obtained before and after 7 days of one-leg immobilization.Results
In both mice and men, short-term skeletal muscle unloading results in molecular marker patterns indicative of increased receptor-mediated mitophagy and decreased mitochondrial biogenesis regulation, before apparent loss of mitochondrial content.Discussion
These results emphasize the early-onset of skeletal muscle disuse-induced mitochondrial remodeling.
SUBMITTER: Leermakers PA
PROVIDER: S-EPMC6900132 | biostudies-literature | 2019 Dec
REPOSITORIES: biostudies-literature
Leermakers Pieter A PA Kneppers Anita E M AEM Schols Annemie M W J AMWJ Kelders Marco C J M MCJM de Theije Chiel C CC Verdijk Lex B LB van Loon Luc J C LJC Langen Ramon C J RCJ Gosker Harry R HR
Muscle & nerve 20191023 6
<h4>Introduction</h4>Physical inactivity significantly contributes to loss of muscle mass and performance in bed-bound patients. Loss of skeletal muscle mitochondrial content has been well-established in muscle unloading models, but the underlying molecular mechanism remains unclear. We hypothesized that apparent unloading-induced loss of muscle mitochondrial content is preceded by increased mitophagy- and decreased mitochondrial biogenesis-signaling during the early stages of unloading.<h4>Meth ...[more]