ArticleCell biochemistry and biophysics2025
Vitamin D Receptor Regulates Oxidative Stress and Apoptosis Via the HIF-1α/HO-1 Pathway in Cardiomyocytes.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Hypoxia-inducible factor-1 (HIF-1) in the molecular mechanisms of liver fibrosis: research progress on its role and therapeutic strategies.Journal of applied genetics · 2026Review
- Bioinformatic Analysis of Apoptosis-Related Genes in Preeclampsia Using Public Transcriptomic and Single-Cell RNA Sequencing Datasets.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Acute myocardial infarction (AMI) is a critical cardiovascular disease with high disability and mortality rates, primarily caused by hypoxic injury to myocardial cells. This study investigates the role of the Vitamin D receptor (VDR) in cardiomyocytes under hypoxic conditions. VDR expression was characterized in human and hypoxic cardiomyocytes isolated from mice. To understand the downstream effects of VDR-related pathways, VDR was modulated using shRNA. RXR expression and localization were measured in hypoxic and sh-VDR cardiomyocytes. Oxidative stress and apoptosis levels were assessed and the effect of Vitamin D treatment was evaluated. VDR expression was found to be downregulated in the serum of AMI patients, similar to the hypoxic cardiomyocytes. Knockdown of VDR induced oxidative stress and apoptosis in normoxic cardiomyocytes, which could not be reversed by vitamin D treatment. Knock-down VDR in cardiomyocytes exposed to hypoxic induced apoptosis and reactive oxygen species via the HIF-1α/HO-1 axis. Overexpression VDR alleviated the expression levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β. Our results indicated that VDR is crucial in reducing myocardial stress and apoptosis during hypoxic injury.
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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.