Spatiotemporal regulation of acute wound healing by the NLRP3 inflammasome: dual roles in macrophage-fibroblast chemotaxis and phenotype during wound repair - PubMed
3 hours ago
- #NLRP3 inflammasome
- #Wound healing
- #Macrophage polarization
- NLRP3 inflammasome plays a critical role in the spatiotemporal regulation of acute wound healing.
- NLRP3 is predominantly expressed in macrophages and neutrophils during the inflammatory phase of wound healing.
- Global deletion of NLRP3 reduces IL-1β, attenuates chemokine signaling, and delays wound closure.
- NLRP3 deficiency may upregulate Wnt and Notch signaling early in the repair phase, reducing fibrosis and promoting appendage regeneration.
- Partial IL-1β blockade in WT mice mimics the NLRP3-null phenotype, while IL-1β reconstitution accelerates healing but increases fibrosis.
- NLRP3 modulates fibroblast phenotype independently of inflammasome activation via a ROS-dependent mechanism.
- NLRP3 has dual-phase regulatory roles: driving chemokine-mediated recruitment during inflammation and enhancing Wnt/Notch signaling later.
- Fibroblasts with high NLRP3 expression engage an inflammasome-independent NLRP3/ROS axis that activates TGF-β/Smad signaling.
- NLRP3 is a potential therapeutic target for modulating inflammatory and regenerative responses in wound healing.