Clearance of senescent cells reverts the cigarette smoke‐induced lung senescence and airspace enlargement in <scp>p16‐3MR</scp> mice

Cigarette smoke (CS) leads to increased oxidative stress, inflammation, and exaggerated senescence, which are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). While role cellular senescence COPD is known, it not clear if removal senescent cells could alleviate symptoms. To test this, we used novel mouse model-p16-3MR, studied effect ganciclovir (GCV)-mediated after CS (3 months) environmental tobacco (ETS) (6 exposure CS. Our results showed reversal CS-induced on clearance p16+ senesced by GCV treatment. Interestingly, via led a decrease neutrophil counts BALF GCV-treated CS-exposed p16-3MR mice, as well CS-mediated airspace enlargement mice. Mice exposed low dose ETS caused insignificant changes SA-β-Gal+ enlargement. Overall, our data provide evidence for lung mice COPD/emphysema pathology with possibility senolytics therapeutic interventions COPD.