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Targeting Senescent Cells as a Treatment for Chronic Obstructive Pulmonary Disease

Researchers have introduced BCLXL-PROTAC, a proteolysis‑targeting chimera that degrades the anti‑apoptotic protein BCLXL in senescent lung cells. In primary small‑airway epithelial cells and fibroblasts from COPD patients, the compound induced caspase‑3‑mediated apoptosis and lowered classic senescence markers such as p21, p16 and SA‑β‑gal. The effect was selective, sparing non‑COPD cells, and precision‑cut lung slices showed reduced p21 expression in the airway epithelium. These data position BCLXL-PROTAC as a promising senolytic candidate to rejuvenate lung tissue and potentially modify COPD progression.