Dermal αSMA⁺ myofibroblasts orchestrate skin wound repair via β1 integrin and independent of type I collagen production.

ABSTRACT: Skin wound repair is essential for organismal survival and failure of which leads to non-healing wounds, a leading health issue worldwide. However, mechanistic understanding of chronic wounds remains a major challenge due to lack of appropriate genetic mouse models. αSMA⁺ myofibroblasts, a unique class of dermal fibroblasts, are associated with cutaneous wound healing but their precise function remains unknown. We demonstrate that genetic depletion of αSMA⁺ myofibroblasts leads to pleiotropic wound healing defects, including lack of reepithelialization and granulation, dampened angiogenesis, and heightened hypoxia, hallmarks of chronic non-healing wounds. Other wound-associated FAP⁺ and FSP1⁺ fibroblasts do not exhibit such dominant functions. Wh

SUBMITTER: McAndrews KM 

PROVIDER: S-EPMC8982612 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature