Cellular senescence is a biological process that prevents abnormal cell proliferation during tissue repair and is associated with the secretion of various factors, such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). SASP promotes tissue repair, regeneration, and development, but excessive accumulation of senescent cells can lead to inflammation, tissue dysfunction, and intractable wounds. This review discusses the role of cellular senescence in wound healing in aged and diabetic skin. In normal skin, senescent cells contribute to wound healing by promoting ECM deposition and epithelialization. However, in aged skin, senescent cells accumulate and impair wound healing by inducing chronic inflammation and fibrosis. In diabetic skin, senescent cells are increased and contribute to delayed wound healing by inhibiting fibroblast proliferation and migration. The accumulation of senescent cells in aged and diabetic skin is associated with impaired wound healing. Senolytic and senomorphic drugs are being explored as potential therapies to target senescent cells and improve wound healing. This review highlights the complex roles of cellular senescence in wound healing and the potential for senotherapeutics to improve outcomes in aged and diabetic skin.Cellular senescence is a biological process that prevents abnormal cell proliferation during tissue repair and is associated with the secretion of various factors, such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). SASP promotes tissue repair, regeneration, and development, but excessive accumulation of senescent cells can lead to inflammation, tissue dysfunction, and intractable wounds. This review discusses the role of cellular senescence in wound healing in aged and diabetic skin. In normal skin, senescent cells contribute to wound healing by promoting ECM deposition and epithelialization. However, in aged skin, senescent cells accumulate and impair wound healing by inducing chronic inflammation and fibrosis. In diabetic skin, senescent cells are increased and contribute to delayed wound healing by inhibiting fibroblast proliferation and migration. The accumulation of senescent cells in aged and diabetic skin is associated with impaired wound healing. Senolytic and senomorphic drugs are being explored as potential therapies to target senescent cells and improve wound healing. This review highlights the complex roles of cellular senescence in wound healing and the potential for senotherapeutics to improve outcomes in aged and diabetic skin.