The Role of Cellular Senescence in Chronic Lung Diseases: Emerging Mechanisms and Translational Perspectives: A Narrative Review

Cellular senescence is one of the major risk factors for the onset and progression of chronic pulmonary diseases. Cellular senescence can be induced by diverse stressors, including genotoxic damage, oncogenic signaling, and therapeutic interventions. These senescent cells communicate via the release of multiple inflammatory molecules known as the Senescence-Associated Secretory Phenotype (SASP), which induces persistent low-grade inflammation and contributes to various chronic inflammatory lung diseases. This review summarizes the basic concepts of cell senescence, its hallmarks, SASP, and the mechanisms of cell senescence in the lung, and its consequences in the development and progression of chronic pulmonary diseases. Current therapeutic strategies include senolytics (e.g., BCL-2 family inhibitors and dasatinib–quercetin) and senomorphics that suppress SASP activity. Future directions in the development of cell- and stage-specific therapies are critical for targeting age-related lung disease with desired outcomes.