Inhibition of prostaglandin-degrading enzyme 15-PGDH rejuvenates aged muscle mass and strength
Open accessAbstract
Maintaining muscle Prostaglandin E2 (PGE2), an eicosanoid that mediates inflammatory responses, also supports the function of muscle stem cells. Palla et al. found that loss of PGE2 in aging mice contributes to loss of muscle and appears to be a consequence of increased activity of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), an enzyme that degrades PGE2 (see the Perspective by Becker and Rudolph). Restoring PGE2 concentrations by inhibiting 15-PGDH in older mice improved muscle function. Decreased activity of 15-PGDH in older animals had beneficial effects that included decreased proteolysis and transforming growth factor–β signaling and increased mitochondrial function and autophagy. The findings reveal a potential therapeutic strategy to help maintain muscle mass and function during aging. Science , this issue p. eabc8059 ; see also p. 462
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shRNA-mediated muscle-specific deletion of 15-PGDH increases aged muscle mass, strength, and exercise performance.
“Increased aged muscle mass, strength, and exercise performance”
From Autophagy in major human diseases (2021) · cites this paper as Palla et al (2021)
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References 72 · Cited by 232
Research works printed but not linked: 1
- [72]Dubowitz V, Sewry C, Oldfors A, Muscle Biopsy: a Practical Approach. (Elsevier Health Sciences, ed. 5th, 2020).
- Authors
- 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.
- Affiliations
- Stanford Medicine (US)
- Stanford University (US)
- Corresponding author
- Blau, H. M.
- Venue
- Science
- Published
- 2021-01-29
- Volume
- 371
- Issue
- 6528
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC7938328
- OpenAlex
- W3112590295
- Cited by
- 232
- References
- 72
- Citations by year
- 2026: 41 · 2025: 46 · 2024: 42 · 2023: 39 · 2022: 38 · 2021: 26
- FWCI
- 8.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5R01AG02096115, 1R01AG069858-01, RHG009674A, K99NS120278, 1S10OD026962-01, 1S10RR026780-01)
- California Institute for Regenerative Medicine (DISC2-10604)
- Li Ka Shing Foundation
- Donald E. and Delia B. Baxter Foundation
- Swiss National Science Foundation (P2EZP3_184231)
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- 15-hydroxyprostaglandin dehydrogenase, prostaglandin E2, muscle aging, muscle mass, muscle strength, eicosanoids, muscle stem cells, proteolysis, TGF-beta signaling, mitochondrial function, autophagy, anti-aging therapy
- MeSH terms
- Autophagic Cell Death, Aging, Animals, Hydroxyprostaglandin Dehydrogenases, Macrophages, Mice, Inbred C57BL, Mitochondria, Muscle, Myofibrils, Rejuvenation, Dinoprostone, Muscle, Skeletal, Mice, Muscle Strength, Sarcopenia
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