Pharmacology of Senolytics for Lung Aging and COPD: An Emerging Therapeutic Frontier

Chronic obstructive pulmonary disease is strongly influenced by accelerated lung aging and an accumulation of senescent cells within airway epithelial and immune compartments. Senescent cells release a spectrum of inflammatory mediators that worsen tissue destruction and impair repair mechanisms. Conventional COPD therapeutics do not adequately address cellular senescence(definition), which has led to growing interest in senolytic drugs that selectively eliminate senescent cells or reduce harmful secretory signaling. Several senolytic candidates, including Dasatinib–Quercetin, Fisetin, Navitoclax, HSP90 inhibitors, and peptide-based approaches, have demonstrated promising effects in preclinical respiratory models. These agents modulate pathways such as BCL-2 inhibition, suppression of PI3K/AKT signaling, activation of mitochondrial apoptosis, or disruption of FOXO4–p53 interactions. Early studies suggest potential for reducing chronic inflammation, restoring epithelial function, and slowing structural deterioration in the lung. Although human evidence remains limited and concerns surrounding toxicity, delivery, and biomarker development persist, senolytics(definition) represent an emerging pharmacological avenue for targeting lung aging and may hold therapeutic value in COPD.