Abstract
Background:
Keloid is a fibrotic disorder of soft tissues secondary to abnormal wound healing. Previous studies have predominantly focused on fibroblasts, yet research on epidermal keratinocytes (KCs) remains limited. Existing evidence indicates that KCs in keloid differ from normal KCs in morphology and transcriptional profiles, with keloid KCs exhibiting EMT-like characteristics. However, the molecular drivers of EMT in keloid KCs and how EMT-primed KCs contribute to keloid pathogenesis and progression remain poorly understood.