Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development

(cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence(definition)-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.