Chronic inflammatory skin disorders are characterized by persistent skin inflammation, impaired barrier function, and frequent recurrence, all of which substantially reduce patients’ quality of life. Traditional studies attribute the pathogenesis of these diseases to immune dysregulation, whereas new evidence indicates that cellular senescence is a key risk factor and a mechanism underlying disease progression. Cellular senescence, defined by irreversible cell cycle arrest, is accompanied by a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and DNA damage. This review systematically outlines the hallmarks, regulatory mechanisms, and inducers of cellular senescence, elucidates its pathological role in representative inflammatory skin disorders, and evaluates emerging therapeutic strategies that target senescent cells. By elucidating the dynamic crosstalk between cellular senescence and inflammatory skin diseases, this review aims to identify novel therapeutic targets and provide new insights into their diagnosis, treatment, and prevention.
Liang et al. (Fri,) studied this question.
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