Role of Senescence-Resumed Proliferation in Keloid Pathogenesis

Senescence-resumed proliferation (SRP) is proposed to be a mechanism associated with the escape of p21-mediated senescence and activation Wnt/β-catenin pathways that enhance malignancy. The keloid genomic landscape shows heavy intersections between TP53 TGF-β signaling. machinery maintain cellular integrity through senescence, apoptosis, autophagy co-regulated stemness, hedgehog, immunomodulation. Our study demonstrated presence SRP how, on transcriptome level, are regulated deliver same fate. proves senescence-associated reprogramming (Wnt/β-catenin pathways) TP53-p21 dysregulations originate from common etiology present novel therapeutic target opportunity.