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Enhanced glycolysis has been linked to fibroblast-myofibroblast transition (FMT) during pulmonary fibrogenesis, however, there is still a lack of pharmaceutical agents to target the metabolic dysregulation. Emerging evidence highlights Vitamin D\u2019s anti-fibrotic potential, yet its role in modulating fibroblast glycolysis and pulmonary fibrosis remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>MRC-5 cells and mouse primary lung fibroblasts treated with TGF-\u03b21 combined with Vitamin D were used to explore the role of vitamin D on fibroblast activation and glycolysis in vitro. Silica and bleomycin-induced pulmonary fibrosis mouse model was established to evaluate the antifibrotic effects of Vitamin D and the glycolysis inhibitor 3-[3-pyridinyl]-1-[4-pyridinyl]-2-propen-1-one (3PO) in vivo. Cell metabolism assays were performed to determine the glycolytic rate. RNA sequencing was utilized to analyse the underlying molecular mechanisms by which Vitamin D affects fibroblast activation and glycolysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Transcriptomic analysis and subsequent experiments demonstrated that TK1 acts as a functional downstream effector of Vitamin D, and its expression was negatively regulated by Vitamin D. Knockdown of TK1 inhibited the profibrotic effects of TGF-\u03b21 by reducing fibroblast glycolysis. Furthermore, 6-phosphofructo-2-kinase\/fructose-2,6-bisphosphatase 3 (PFKFB3), a key driver of glycolysis, was identified as a target of TK1. Mechanistically, Vitamin D could reduce the expression of TK1, thereby partly blocking fibroblast glycolysis and activation by inhibiting PFKFB3. In a murine model of silica or bleomycin-induced fibrosis, both Vitamin D and 3PO treatment alleviated pulmonary fibrosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings revealed that Vitamin D could attenuate pulmonary fibrosis by blocking fibroblast glycolysis and FMT through the TK1-PFKFB3 pathway. Vitamin D supplementation or targeting fibroblast glycolysis could be promising treatment strategies for pulmonary fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12967-025-07298-1","type":"journal-article","created":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T13:28:07Z","timestamp":1776864487000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Vitamin D attenuates the progression of pulmonary fibrosis via inhibiting thymidine kinase 1\/PFKFB3-driven glycolysis"],"prefix":"10.1186","volume":"24","author":[{"given":"Huanyu","family":"Yang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengjia","family":"Han","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keye","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianghan","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenkang","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,22]]},"reference":[{"key":"7298_CR1","doi-asserted-by":"publisher","first-page":"s334","DOI":"10.1378\/chest.122.6_suppl.334S","volume":"122","author":"FH Green","year":"2002","unstructured":"Green FH. 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