biostudies-literatureUnknown50(2)Lehmann MHelmholtz Munich Postdoctoral ProgramHelmholtz AssociationWhitaker International Scholar FellowshipGerman Center of Lung ResearchIdiopathic pulmonary fibrosis (IPF) is a devastating lung disease with poor prognosis and limited therapeutic options. The incidence of IPF increases with age, and ageing-related mechanisms such as cellular senescence have been proposed as pathogenic drivers. The lung alveolar epithelium represents a major site of tissue injury in IPF and senescence of this cell population is probably detrimental to lung repair. However, the potential pathomechanisms of alveolar epithelial cell senescence and the impact of senolytic drugs on senescent lung cells and fibrosis remain unknown. Here we demonstrate that lung epithelial cells exhibit increased <i>P16</i> and <i>P21</i> expression as well as senescence-associated β-galactosidase activity in experimental and human lung fibrosis tissue and primary The European respiratory journal1602367https://www.ebi.ac.uk/biostudies/studies/S-EPMC5593348biostudies-literatureSenolytic drugs target alveolar epithelial cell function and attenuate experimental lung fibrosis <i>ex vivo</i>.PMC5593348Mutze KKonigshoff MKorfei MKlee SLindner MLehmann MSkronska-Wasek WWagner DEGunther AOta CCosta RSchiller HBAlsafadi HNfalseSenolytic drugs target alveolar epithelial cell function and attenuate experimental lung fibrosis <i>ex vivo</i>.Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with poor prognosis and limited therapeutic options. The incidence of IPF increases with age, and ageing-related mechanisms such as cellular senescence have been proposed as pathogenic drivers. The lung alveolar epithelium represents a major site of tissue injury in IPF and senescence of this cell population is probably detrimental to lung repair. However, the potential pathomechanisms of alveolar epithelial cell senescence and the impact of senolytic drugs on senescent lung cells and fibrosis remain unknown. Here we demonstrate that lung epithelial cells exhibit increased <i>P16</i> and <i>P21</i> expression as well as senescence-associated β-galactosidase activity in experimental and human lung fibrosis tissue and primary 2017-01-01T00:00:00Z2017 Aug2026-06-11T06:06:16.884Z2026-06-11T03:12:50.204ZS-EPMC55933482877504410.1183/13993003.02367-2016