Arylsulfatase K attenuates airway epithelial cell senescence in COPD by regulating parkin-mediated mitophagy.

ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung condition characterized by irreversible airflow limitation, primarily due to cigarette smoke (CS) exposure. Emerging research underscores the pivotal role of cellular senescence in the pathogenesis of COPD. The arylsulfatase family, known for its involvement in various age-related diseases, has yet to be investigated in the context of COPD. This study investigated the role of the arylsulfatase family, particularly ARSK, in COPD pathogenesis. Bioinformatics analysis and clinical validation revealed significantly reduced ARSK expression in COPD patients' lungs, especially in airway epithelium. ARSK overexpression alleviated CS-induced epithelial cellular senescence and improved mitophagy and mitochondrial function, while AR

SUBMITTER: Yang R 

PROVIDER: S-EPMC12344987 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature