Fibroadipogenic progenitor-secreted prostaglandin E2 coordinates stem cell fate via autocrine and paracrine crosstalk in healthy and dystrophic muscle - PubMed
4 hours ago
- #stem cell niche
- #fibrosis
- #muscle regeneration
- Fibroadipogenic progenitors (FAPs) are a key source of prostaglandin E2 (PGE2) in resting and regenerating muscle.
- FAP-secreted PGE2 regulates muscle stem cells via paracrine signaling, supporting their maintenance and post-injury proliferation.
- PGE2 also acts autocrinely on FAPs to control their fate decisions, including apoptosis, preventing excessive accumulation.
- Inhibition of PGE2 synthesis (e.g., with NSAIDs or COX2 ablation in FAPs) leads to increased FAP numbers, fibrosis, and impaired regeneration.
- PGE2 administration rescues these defects, highlighting its therapeutic potential for muscle injury and dystrophy.
- In Duchenne muscular dystrophy models, FAPs show impaired PGE2 production; restoring PGE2 reduces fibrosis and improves muscle strength.