Abstract
BackgroundAging leads to decreased skeletal muscle function in mammals and is associated with a progressive loss of muscle mass, quality and strength. Age-related muscle loss (sarcopenia) is an important health problem associated with the aged population.ResultsWe investigated the alteration of genome-wide transcription in mouse skeletal muscle tissue (rectus femoris muscle) during aging using a high-throughput sequencing technique. Analysis revealed significant transcriptional changes between skeletal muscles of mice at 3 (young group) and 24 (old group) months of age. Specifically, genes associated with energy metabolism, cell proliferation, muscle myosin isoforms, as well as immune functions were found to be altered. We observed several interesting gene expression changes in the elderly, many of which have not been reported before.ConclusionsThose data expand our understanding of the various compensatory mechanisms that can occur with age, and further will assist in the development of methods to prevent and attenuate adverse outcomes of aging.
Highlights
Aging leads to decreased skeletal muscle function in mammals and is associated with a progressive loss of muscle mass, quality and strength
The results showed that the genes involved in muscle functions and metabolism were among the largest transcriptional changes observed in aged animals
Genes associated with type I muscle fibers, Tnnt1 (Troponin T1, slow skeletal type) and Atp2a2 (ATPase sarcoplasmic/ endoplasmic reticulum Ca2+ transporting 2), were up-regulated in 24-month-old muscle (2.53- and 1.93- fold respectively), indicating a fast-to-slow muscle fiber transition during aging
Summary
Aging leads to decreased skeletal muscle function in mammals and is associated with a progressive loss of muscle mass, quality and strength. Age-related muscle loss (sarcopenia) is an important health problem associated with the aged population. Aging is a process whereby various changes were accumulated over time, resulting in dysfunction in molecules, cells, tissues and organs. Some protein products can trigger senescence in tissues or organs through the circulation system; others are potential biomarkers of aging that are released into blood circulation. Activation and overexpression of SIRT1 reduces the oxidative stress and inflammation associated with ameliorating diseases, such as vascular endothelial disorders, neurodegenerative diseases, as well as skeletal muscle aging [7,8,9,10]. The aging phenotype is extremely complicated and there is currently no reliable and universal marker for aging
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