Fibroblasts (FB) are widely distributed in the interstitial tissues of various organs and play a central role in skin wound healing.Due to their high plasticity,FB can respond to signals from the tissue damage microenvironment,undergoing phenotypic changes and dynamically maintaining tissue homeostasis and structural integrity.As a heterogeneous and functionally diverse cell type,FB not only regulate inflammation and angiogenesis,but also exhibit stem cell-like properties, playing a critical role in skin wound healing and pathological scar formation. Under physiological conditions, FB are moderately activated, synthesizing and remodeling extracellular matrix components, such as collagen, to promote tissue regeneration. Once healing is complete, they either undergo apoptosis or return to a quiescent state to maintain collagen turnover balance. However, during pathological scar formation, FB remain persistently activated and evade apoptosis, leading to abnormal collagen deposition and extracellular matrix components disorganization, ultimately resulting in functional impairment. This review primarily discusses the mechanisms by which FB contribute to skin wound healing and scar formation, aiming to clarify the biological behaviors of FB at different stages of wound healing. The goal is to provide new theoretical insights and potential therapeutic targets for clinical interventions in skin wound repair and the prevention of pathological scarring.