Research progress in the relationship between cellular senescence and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a common and frequently occurring disease that seriously threatens human health. It has been proposed that patients with COPD exhibit premature biological aging. Cellular senescence refers to a state of irreversible, permanent cell cycle arrest and is the cellular basis of organismal aging. The relationship between cellular senescence and COPD is close and complex. Oxidative stress caused by tobacco smoke, the most important risk factor for COPD, is closely associated with multiple mechanisms of senescence, leading to cellular senescence and the senescence-associated secretory phenotype (senescence-associated secretory phenotype,SASP). Cellular senescence participates in the onset and progression of chronic airway inflammation and emphysema and is associated with COPD comorbidities. Hypoxia, the inflammatory microenvironment, recurrent infections, and other factors in COPD can promote cellular senescence and its further accumulation; cellular senescence may be both a cause of COPD onset and a consequence of its progression; therapies targeting cellular senescence may provide new therapeutic strategies for COPD, and here we briefly review research progress on the role of cellular senescence in the onset and progression of COPD.