The article reviews the role of cellular senescence in wound healing in normal, aged, and diabetic skin. Cellular senescence, characterized by irreversible cell cycle arrest, is induced by various stressors and plays a crucial role in tissue homeostasis and pathophysiology. Senescent cells, through the secretion of senescence-associated secretory phenotypes (SASPs), can promote or inhibit wound healing depending on the context. In normal skin, senescent fibroblasts and mesenchymal cells in subcutaneous white adipose tissue (sWAT) contribute to optimal wound closure by secreting PDGF-AA, which promotes myofibroblast differentiation. However, in aged skin, the accumulation of senescent cells leads to delayed wound healing due to increased inflammation and fibrosis. In diabetic skin, senescent fibroblasts and macrophages inhibit wound healing through CXCL2-CXCR2 signaling, contributing to diabetic ulcers. The accumulation of senescent mesenchymal cells in sWAT also impairs wound healing. Therapeutic interventions targeting cellular senescence, such as senolytics and senomorphics, show promise in improving wound healing, but further research is needed to understand the complex roles of senescent cells in different skin conditions.The article reviews the role of cellular senescence in wound healing in normal, aged, and diabetic skin. Cellular senescence, characterized by irreversible cell cycle arrest, is induced by various stressors and plays a crucial role in tissue homeostasis and pathophysiology. Senescent cells, through the secretion of senescence-associated secretory phenotypes (SASPs), can promote or inhibit wound healing depending on the context. In normal skin, senescent fibroblasts and mesenchymal cells in subcutaneous white adipose tissue (sWAT) contribute to optimal wound closure by secreting PDGF-AA, which promotes myofibroblast differentiation. However, in aged skin, the accumulation of senescent cells leads to delayed wound healing due to increased inflammation and fibrosis. In diabetic skin, senescent fibroblasts and macrophages inhibit wound healing through CXCL2-CXCR2 signaling, contributing to diabetic ulcers. The accumulation of senescent mesenchymal cells in sWAT also impairs wound healing. Therapeutic interventions targeting cellular senescence, such as senolytics and senomorphics, show promise in improving wound healing, but further research is needed to understand the complex roles of senescent cells in different skin conditions.