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Palla, A R; Ravichandran, M; Wang, Y X; Alexandrova, L; Yang, A V; Kraft, P; Holbrook, C A; Schürch, C M; Ho, A T V; Blau, H M
Science (American Association for the Advancement of Science), 01/2021, Volume: 371, Issue: 6528Journal Article
Treatments are lacking for sarcopenia, a debilitating age-related skeletal muscle wasting syndrome. We identifed increased amounts of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), the prostaglandin E (PGE )-degrading enzyme, as a hallmark of aged tissues, including skeletal muscle. The consequent reduction in PGE signaling contributed to muscle atrophy in aged mice and results from 15-PGDH-expressing myofibers and interstitial cells, such as macrophages, within muscle. Overexpression of 15-PGDH in young muscles induced atrophy. Inhibition of 15-PGDH, by targeted genetic depletion or a small-molecule inhibitor, increased aged muscle mass, strength, and exercise performance. These benefits arise from a physiological increase in PGE concentrations, which augmented mitochondrial function and autophagy and decreased transforming growth factor-β signaling and activity of ubiquitin-proteasome pathways. Thus, PGE signaling ameliorates muscle atrophy and rejuvenates muscle function, and 15-PGDH may be a suitable therapeutic target for countering sarcopenia.
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