2026-07-21T16:13:42Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/160612024-11-29T22:49:25Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Piñeiro-Hermida, Sergio author Martinez Rodriguez, Paula author Bosso, Giuseppe author Flores, Juana María author Saraswati, Sarita author Connor, Jane author Lemaire, Raphael author Blasco, MA author 2022-10-06 TRF1 is an essential component of the telomeric protective complex or shelterin. We previously showed that dysfunctional telomeres in alveolar type II (ATII) cells lead to interstitial lung fibrosis. Here, we study the lung pathologies upon telomere dysfunction in fibroblasts, club and basal cells. TRF1 deficiency in lung fibroblasts, club and basal cells induced telomeric damage, proliferative defects, cell cycle arrest and apoptosis. While Trf1 deletion in fibroblasts does not spontaneously lead to lung pathologies, upon bleomycin challenge exacerbates lung fibrosis. Unlike in females, Trf1 deletion in club and basal cells from male mice resulted in lung inflammation and airway remodeling. Here, we show that depletion of TRF1 in fibroblasts, Club and basal cells does not lead to interstitial lung fibrosis, underscoring ATII cells as the relevant cell type for the origin of interstitial fibrosis. Our findings contribute to a better understanding of proper telomere protection in lung tissue homeostasis. Nat Commun. 2022;13(1):5656. 10.1038/s41467-022-32771-6 2041-1723 Nature communications 36202783 http://hdl.handle.net/20.500.12105/16061 Consequences of telomere dysfunction in fibroblasts, club and basal cells for lung fibrosis development.