Research
Mixed
Mitochondrial dysfunction acts as a primary driver of skeletal muscle atrophy by triggering catabolic signaling pathways that promote the expression of muscle atrophy genes and increasing oxidative stress.
To support muscle mass, prioritize activities that improve mitochondrial health, such as regular aerobic and resistance exercise. These interventions help regulate mitochondrial function and may prevent or treat muscle atrophy, especially in aging or diseased states.
GoodSupportsHIGH confidence
Mitochondrial dysfunction triggers catabolic signaling pathways, which then will feed back to the nucleus to promote the expression of muscle atrophy genes [18].
Why this rating
Review of multiple studies including clinical trials and in vivo models; strong mechanistic evidence.
Source
Mitochondrial dysfunction: roles in skeletal muscle atrophy
Xin Chen et al. · Journal of Translational Medicine · 2023
DOI 10.1186/s12967-023-04369-z
narrative_reviewCited 272×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Targeted modulation of mitochondrial function through drugs, exercise, diet, gene therapy, stem cell therapy, and physical therapy can prevent or treat skeletal muscle atrophy.Good
- Inflammation and oxidative stress are crucial triggering factors in skeletal muscle atrophy, leading to increased proteolysis and reduced protein synthesis.Good
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