ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
Muscle Injuries Induce a Prostacyclin-PPARγ/PGC1a-FAO Spike That Boosts Regeneration.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Dietary omega-6 arachidonic acid and omega-3 docosahexaenoic acid supplementation differentially impact skeletal muscle inflammaging in mice.bioRxiv : the preprint server for biology · 2026Article
- Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.Frontiers in pharmacology · 2026Article
- Etifoxine drives macrophage M2 polarization via Schwann cell-derived progesterone activation of PPARγ to accelerate peripheral nerve repair.Frontiers in cellular neuroscience · 2026Article
- PGC-1α: key regulator of mitochondrial biogenesis and cellular differentiation in metabolic and regenerative tissues.Cell & bioscience · 2025Review
- Spatially resolved multi-omics of human metabolic dysfunction-associated steatotic liver disease.Nature genetics · 2025Article
- Gut symbiont-derived ursodeoxycholic acid promotes fatty acid oxidation to protect against renal ischemia-reperfusion injury.Cell reports. Medicine · 2025Article
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- Genetically Engineered Hypoimmune Human Muscle Progenitor Cells Can Reduce Immune Rejection.Cell proliferation · 2025Article
- The role of PPARγ in cancer cachexia: friend or foe?Frontiers in endocrinology · 2025Review
- Review
- Integrating Physical and Biochemical Cues for Muscle Engineering: Scaffolds and Graft Durability.Bioengineering (Basel, Switzerland) · 2024Review
- The metabaging cycle promotes non-metabolic chronic diseases of ageing.Cell proliferation · 2024Article
- Muscle Injuries Induce a Prostacyclin-PPARγ/PGC1a-FAO Spike That Boosts Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
It is well-known that muscle regeneration declines with aging, and aged muscles undergo degenerative atrophy or sarcopenia. While exercise and acute injury are both known to induce muscle regeneration, the molecular signals that help trigger muscle regeneration have remained unclear. Here, mass spectrometry imaging (MSI) is used to show that injured muscles induce a specific subset of prostanoids during regeneration, including PGG1, PGD2, and the prostacyclin PGI2. The spike in prostacyclin promotes skeletal muscle regeneration via myoblasts, and declines with aging. Mechanistically, the prostacyclin spike promotes a spike in PPARγ/PGC1a signaling, which induces a spike in fatty acid oxidation (FAO) to control myogenesis. LC-MS/MS and MSI further confirm that an early FAO spike is associated with normal regeneration, but muscle FAO became dysregulated during aging. Functional experiments demonstrate that the prostacyclin-PPARγ/PGC1a-FAO spike is necessary and sufficient to promote both young and aged muscle regeneration, and that prostacyclin can synergize with PPARγ/PGC1a-FAO signaling to restore aged muscles' regeneration and physical function. Given that the post-injury prostacyclin-PPARγ-FAO spike can be modulated pharmacologically and via post-exercise nutrition, this work has implications for how prostacyclin-PPARγ-FAO might be fine-tuned to promote regeneration and treat muscle diseases of aging.
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Registered trials
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