research TGFβ ‐mediated inhibition of hypodermal adipocyte progenitor differentiation promotes wound‐induced skin fibrosis
This study establishes a wound-induced skin fibrosis (WISF) mouse model that mimics human fibrotic skin diseases, characterized by excessive collagen deposition and loss of dermal adipocytes. The research identifies TGFβ as a key signal that inhibits the differentiation of hypodermal interstitial adipocyte progenitors (HI-APs) into adipocytes, instead promoting their fibrogenic potential. The study shows that blocking TGFβ signaling can reduce the abundance of extracellular matrix-producing adipocyte progenitors, suggesting that targeting HI-APs and adipogenesis could lead to new treatments for fibrotic skin conditions. Analysis of human scleroderma tissues supports these findings, showing a negative correlation between adipogenic and fibrogenic gene expression.
