Largely Distinct Post‐Translational Modifications Differentiate Skeletal Muscle Wasting Caused by Cancer, Dexamethasone and Aging

These analyses identify atrophy-associated PTMs that provide refined biomarkers for fingerprinting the atrophic stimulus. Although most PTMs are stimulus-specific, P27 dihydroxylation of Lrpprc declines during muscle wasting induced by cancer, dexamethasone and aging, suggesting that this is a general atrophy marker. Experimental up-regulation of the atrophy-mimicking variant Lrpprc^P27A reduces muscle force compared to wild-type Lrpprc in young and old mice, suggesting that atrophy-associated P27 dihydroxylation contributes to disease-associated muscle weakness.