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Targeting p16INK4a reverses alveolar epithelial cell dysfunction and induces lung regeneration in emphysema

Ribeiro Baptista, B.; Toigo, M.; Justeau, G.; Abou-atmeh, P.; De Freitas Castro, T.; Zysman, M.; Thiebaut De Menonville, C.; Audureau, E.; Schnyder, K.; Wang, H.; Hu, Y.; Koenigshoff, M.; Lanone, S.; Chabot, F.; Zana-Taieb, E.; Jourdan Le Saux, C.; Lehmann, M.; Derumeaux, G.; Boczkowski, J.; Gote-Schniering, J.; Boyer, L.

2025-09-07 cell biology
10.1101/2025.09.05.674489 bioRxiv
Show abstract

Pulmonary emphysema involves impaired regenerative capacity of alveolar type 2 epithelial cells (AT2), the main progenitor cells in alveoli. However, the mechanisms underlying dysfunctional epithelial repair remain unclear. In a mouse model of elastase-induced emphysema, we observed an accumulation of activated AT2s in the lung, associated with an overexpression of p16INK4a (p16), a cell cycle inhibitor known to influence stem cell fate. Deletion of p16 promoted the transition of AT2 into alveolar type 1 (AT1) cells, resulting in tissue regeneration in both mice and alveolar organoids. Pharmacological targeting of the p16 pathway using senolytic agents recapitulate this regenerative effect, further supporting the role of p16 as a key brake on epithelial plasticity. These findings demonstrate that alveolar epithelial cell dysfunction can be reversed by p16 deletion or by eliminating p16+ cells, thereby reactivating the AT2-to-AT1 transition and promoting endogenous alveolar regeneration. This work identifies the p16 pathway as a promising therapeutic target for restoring damaged alveoli in emphysema.

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