Abstract
Sjögren's syndrome (SS) is an autoimmune disease primarily affecting exocrine glands, characterized by dry mouth and eyes, with an unclear pathogenesis. Recent studies suggest that salivary gland (SG) cell senescence is critical in SS pathogenesis. The senescence mechanism may serve as a critical pathological nexus linking molecular abnormalities to clinical phenotypes. Under assaults from infections, environmental factors, and immune dysregulation, SG cells undergo oxidative stress, telomere shortening, and DNA damage, leading to senescence. Senescent cells lose proliferative capacity and secrete senescence-associated cytokines, triggering inflammation and immune responses that exacerbate disease progression. Elucidating the mechanisms of SG cell senescence may advance our understanding of SS pathogenesis and identify novel therapeutic targets, offering new avenues for SS treatment.