Guijarro, TrinidadMagro-Lopez, EsmeraldaManso, JoanaGarcia-Martinez, RicardoFernández-Aceñero, María JesúsListe-Noya, IsabelZambrano, Alberto2019-05-212019-05-212018Mol Med. 2018 Dec 19;24(1):64.1076-1551http://hdl.handle.net/20.500.12105/7644BACKGROUND: The multiple biological effects of vitamin D and its novel activities on inflammation and redox homeostasis have raised high expectations on its use as a therapeutic agent for multiple fibrogenic conditions. We have assessed the therapeutic effects of 1α,25-Dihydroxyvitamin D3, the biologically active form of vitamin D, in the context of lung fibrosis. METHODS: We have used representative cellular models for alveolar type II cells and human myofibroblasts. The extension of DNA damage and cellular senescence have been assessed by immunofluorescence, western-blot and senescence-associated β-galactosidase activity. We have also set up a murine model for lung fibrosis by intraperitoneal injections of bleomycin. RESULTS: Vitamin D induces cellular senescence in bleomycin-treated alveolar epithelial type II cells and aggravates the lung pathology induced by bleomycin. These effects are probably due to an alteration of the cellular DNA double-strand breaks repair in bleomycin-treated cells. CONCLUSIONS: The detrimental effects of vitamin D in the presence of a DNA damaging agent might preclude its use as an antifibrogenic agent for pulmonary fibrosis characterized by DNA damage occurrence and cellular senescence.engVoRhttp://creativecommons.org/licenses/by/4.0/A549 CellsAnimalsBleomycinCellular SenescenceEpithelial CellsFemaleHumansLungMice, Inbred C57BLMyofibroblastsPulmonary FibrosisVitamin DDNA DamageAtribución 4.0 Internacional305675042416410.1186/s10020-018-0064-z1528-3658Molecular medicine (Cambridge, Mass.)open access