Smurf2-Induced Degradation of SMAD2 Causes Inhibition of Hair Follicle Stem Cell Differentiation

This study investigated the role of SMAD2 in hair follicle stem cell (HFSC) differentiation and its interaction with Smurf2. It was found that SMAD2 overexpression in HFSCs promoted differentiation and apoptosis while inhibiting cell proliferation. Smurf2 facilitated the ubiquitination and degradation of SMAD2, leading to reduced SMAD2 expression, which in turn decreased NANOG and DNMT1 expression, suppressing differentiation and apoptosis but enhancing proliferation. In a mouse model, increased Smurf2 expression hindered epidermal wound healing by disrupting the SMAD2/NANOG/DNMT1 pathway. The findings suggested that restoring SMAD2 could be a potential target for promoting HFSC differentiation and improving skin wound healing.