ArticleThe Journal of endocrinology2009
Vitamin D reduces the expression of collagen and key profibrotic factors by inducing an antifibrotic phenotype in mesenchymal multipotent cells.
Article in The Journal of endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Fatty liver index (FLI): more than a marker of hepatic steatosis.Journal of physiology and biochemistry · 2024Pooled it
- Trial
- Weekly regimen of vitamin D supplementation is more efficacious than stoss regimen for treatment of vitamin D deficiency in children with chronic liver diseases.European journal of pediatrics · 2018Trial
- Trial
- Vitamin D Supplementation Modulates Base Excision Repair (BER) Machinery in Systemic Sclerosis: A Prospective Longitudinal Study.Biochemical genetics · 2026Article
- The Role of Gut Microbiota in Liver Regeneration After Partial Hepatectomy: New Evidence From Animal and Human Studies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Modulation of Cardiometabolic Risk by Vitamin D and K2: Simple Supplementation or Real Drug? Uncovering the Pharmacological Properties.International journal of molecular sciences · 2025Review
- Article
- Pathogenesis, Non-Invasive Assessments and Treatment of Hepatic Fibrosis in Autoimmune Liver Diseases.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Review
- Potential therapeutic impacts of vitamin D on hypothyroid-induced heart and kidney fibrosis and oxidative status in male rat.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Unveiling the Link: The Potential Roles of Vitamin D in Keloid Pathophysiology.Experimental dermatology · 2025Review
- 25OH vitamin D3 in biliary atresia: a simple and under-utilised diagnostic method.Frontiers in pediatrics · 2025Article
- Key genes of vitamin D metabolism and their roles in the risk and prognosis of cancer.Frontiers in genetics · 2025Review
- Vitamin D Receptor Regulates Liver Regeneration After Partial Hepatectomy in Male Mice.Endocrinology · 2024Article
- Vitamin D and Cardiovascular Diseases: From Physiology to Pathophysiology and Outcomes.Biomedicines · 2024Review
- Approaching the Sarcopenic Patient with Nonalcoholic Steatohepatitis-related Cirrhosis.Journal of clinical and translational hepatology · 2024Review
- Article
- Can Vitamin D Levels Alter the Effectiveness of Short-Term Facelift Interventions?Healthcare (Basel, Switzerland) · 2023Article
- 1,25-Dihydroxycholecalciferol down-regulates 3-mercaptopyruvate sulfur transferase and caspase-3 in rat model of non-alcoholic fatty liver disease.Journal of molecular histology · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Hypovitaminosis D is an important public health problem. Serum 25-hydroxyvitamin D (25-OHD) is now recognized as an independent predictor for cardiovascular and related diseases (CVD) as well as other chronic medical conditions. However, the biologic pathways through which these effects are mediated remain poorly understood. We hypothesized that exposing mesenchymal multipotent cells (MMCs) to the active form of vitamin D would increase the expression of selected antifibrotic factors that in turn would ameliorate the progression of chronic diseases. MMCs were primed with 5'-azacytidine to induce a fibrotic phenotype and then treated with active vitamin D (1,25D) or ethanol <0.1% as vehicle in a time course manner (30 min, 1, 5, and 24 h, and for 4 and 7 days). The addition of 1,25D to MMCs promotes: a) increased expression and nuclear translocation of the vitamin D receptor; b) decreased expression of TGFB1 and plasminogen activator inhibitor (SERPINE1), two well-known profibrotic factors; c) decreased expression of collagen I, III and other collagens isoforms; and d) increased expression of several antifibrotic factors such as BMP7 a TGFB1 antagonist, MMP8 a collagen breakdown inducer and follistatin, an inhibitor of the profibrotic factor myostatin. In conclusion, the addition of 1,25D to differentiated MMCs displays a decreased profibrotic signaling pathway and gene expression, leading to decrease in collagen deposition. This study highlights key mechanistic pathways through which vitamin D decreases fibrosis, and provides a rationale for studies to test vitamin D supplementation as a preventive and/or early treatment strategy for CVD and related fibrotic disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.