ArticleNutrients2023
Vitamin D Attenuates Ulcerative Colitis by Inhibiting ACSL4-Mediated Ferroptosis.
Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Vitamin D and Intestinal Diseases: Impact on Intestinal Immunity and Gut Barrier Function.Diseases (Basel, Switzerland) · 2026Review
- Postbiotic Nagqu4580 Attenuates Ulcerative Colitis and Suppresses Ferroptosis in Association with the Microbiota-Tryptophan-AhR/Nrf2 Axis.Nutrients · 2026Article
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Liposomal Vitamin C as a Modulator of the Efficacy of Ceralasertib Therapy in Ovarian Cancer.International journal of molecular sciences · 2026Article
- MicroRNAs as novel therapeutic targets against inflammatory bowel disease through modulation of ferroptosis.Clinical and experimental medicine · 2026Review
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Electroacupuncture ameliorates ulcerative colitis by suppressing ferroptosis via the JAK2/STAT3 signaling pathway.Chinese medicine · 2026Article
- Inflammatory bowel diseases: pathological mechanisms and therapeutic perspectives.Molecular biomedicine · 2026Review
- Combined therapy with vitamin D, mesalazine, and microecological preparations improves clinical outcome in ulcerative colitis.American journal of translational research · 2026Article
- Identification and Analysis of Biomarkers Associated With Lipid Metabolism and Ferroptosis in Ulcerative Colitis.Journal of immunology research · 2026Article
- Metabolic reprogramming in ulcerative colitis: integrating dietary drivers, pathogenesis, and therapeutic advances.Frontiers in immunology · 2026Review
- Protective Effects of Betanin in Acute and Subacute Periods in Experimental Colitis Induced by Trinitrobenzene Sulfonic Acid.Nutrients · 2025Article
- Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate.Gut microbes · 2025Article
- Transcriptomic exploration of key genes related to mitochondria and ferroptosis in inflammatory bowel disease and experimental validation.Scientific reports · 2025Article
- Dysregulated programmed cell death of intestinal epithelial cells in ulcerative colitis: Molecular mechanisms and novel therapeutic interventions (Review).International journal of molecular medicine · 2025Review
- Hepatic ferroptosis induced by Clonorchis sinensis exacerbates liver fibrosis.PLoS neglected tropical diseases · 2025Article
- Article
- The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.European journal of medical research · 2025Review
- Targeting novel regulated cell death: disulfidptosis in cancer immunotherapy with immune checkpoint inhibitors.Biomarker research · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWith environmental and lifestyle changes, recent epidemiological studies have shown that the prevalence of Ulcerative Colitis (UC) is on the rise, while treatment options are limited. There is an urgent need to explore the underlying mechanisms of vitamin D (VD) as an effective treatment.
methodsDextran sulfate sodium-induced mice and lipopolysaccharide-induced HCT116 cells were used to establish the classic UC models in vivo and in vitro, respectively. Typical symbols of inflammation (IL-6, COX-2), oxidative stress (MDA, MPO, GSH), and ferroptosis (ACSL4, GPX4, SLC7A11, and Iron) were analyzed by Western blot, Immunohistochemistry, RT-PCR, and relative assay kits. The inflammation factors and oxidative stress injury of cells transfected with ACSL4
resultsVitamin D attenuated the levels of COX-2, IL-6, Iron, MDA, and MPO and improved SOD1 and GSH contents in DSS + VD and LPS + VD groups, compared with model groups. Ferrostatin-1 (Fer-1) could relieve the levels of COX-2, IL-6, Iron, MDA, and MPO while increasing the contents of SOD1 and GSH in DSS + Fer-1 and LPS + Fer-1 compared to model groups. VD downregulated the expression of ACSL4 and upregulated GPX4 in tissues and cells. After transfected with ACSL4
conclusionsVitamin D can relieve UC by inhibiting ferroptosis both in mice and in cells through the negative regulation of ACSL4, providing new insight into the therapeutic function of VD on UC.
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