ArticleBMC gastroenterology2020
25(OH) D3 alleviate liver NK cytotoxicity in acute but not in chronic fibrosis model of BALB/c mice due to modulations in vitamin D receptor.
Article in BMC gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Vitamin D3 Enhances Endothelial Function and Improves Vascular Reactivity in an Experimental Model of Type 2 Diabetes Mellitus in Rats.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Osteopontin neutralization increases vitamin D receptors on NKT cells and ameliorates liver fibrosis by promoting their activity.Frontiers in pharmacology · 2024Article
- Restoring natural killer cell activity in lung injury with 1,25-hydroxy vitamin DFrontiers in immunology · 2024Article
- The immune and metabolic treatment approach of using testosterone on mice models of liver injury.Frontiers in pharmacology · 2023Article
- Targeting VDR-RXR heterodimerization in neurodegenerative diseases: a hypothetical framework for combined vitamin DFrontiers in neurologyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLow 25-Hydroxy-vitamin-D; "25(OH)-D3" serum and vitamin D receptor (VDR) levels were recently correlated to advanced fibrosis. However, VDR mechanism in liver fibrosis modulations is not well understood. In this study, we aimed to evaluate changes in liver NK cells cytotoxicity due to modulations in VDR in CCl
methodsCarbon-tetrachloride (CCl
resultsSystemic inflammation and hepatic-fibrosis increased along 4 weeks of CCl
conclusionVitamin D alleviate liver NK cytotoxicity in acute but not in chronic fibrosis model due to modulations in vitamin D receptor and calcium. Hypercalcemia associated with late fibrosis may inhibited VDR levels, however, may not explain the profibrogenic effects of vitamin D.
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Registered trials
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