Research
Hormonal
Muscle atrophy in catabolic conditions (cancer, diabetes, inactivity) is driven by the upregulation of 'atrogines' like MuRF1 and Atrogin-1, which target structural proteins for degradation via the ubiquitin-proteasome system.
Muscle loss during illness or inactivity is not just 'passive'; your body actively activates specific genes (like MuRF1 and Atrogin-1) to break down muscle protein. This process is driven by stress hormones and inflammation. Preventing or reversing this requires addressing the underlying catabolic drivers, not just 'resting'.
StrongSupportsHIGH confidence
The comparison of the gene expression profiles of muscles from different catabolic conditions led to the identification of a common set of genes that were named atrogenes... Among these atrophy-related genes there are several that belong to the major cellular degradation systems, the ubiquitin–proteasome and autophagy–lysosome.
Why this rating
Extensive review of knockout mouse models and gene expression data.
Source
Mechanisms of muscle atrophy and hypertrophy: implications in health and disease
Roberta Sartori et al. · Nature Communications · 2021
DOI 10.1038/s41467-020-20123-1
narrative_reviewCited 902×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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