2026-07-21T15:10:29Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/76442025-06-13T09:06:32Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19617

00925njm 22002777a 4500 dc Guijarro, Trinidad author Magro-Lopez, Esmeralda author Manso, Joana author Garcia-Martinez, Ricardo author Fernández-Aceñero, María Jesús author Liste-Noya, Isabel author Zambrano, Alberto author 2018 BACKGROUND: 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. Mol Med. 2018 Dec 19;24(1):64. 10.1186/s10020-018-0064-z 1528-3658 1076-1551 Molecular medicine (Cambridge, Mass.) 30567504 http://hdl.handle.net/20.500.12105/7644 Detrimental pro-senescence effects of vitamin D on lung fibrosis