ArticleScientific reports2025
1,25(OH)₂D₃ inhibits ferroptosis in nucleus pulposus cells via VDR signaling to mitigate lumbar intervertebral disc degeneration.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Precision mitochondrial delivery for tissue repair in intervertebral disc degeneration.Journal of nanobiotechnology · 2026Article
- Lactate Metabolism in the Intervertebral Disc: Mechanistic Insights and Pathological Implications.Biomolecules · 2026Review
- miR-188-5p accelerates intervertebral disc degeneration by mediating P4HB to regulate ferroptosis in nucleus pulposus cells.European journal of medical research · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Lumbar intervertebral disc degeneration (LIDD) serves as a principal contributor to low back pain, a condition that poses considerable global health and socioeconomic challenges. Recent studies have emphasized the significance of ferroptosis, an iron-dependent mechanism of programmed cell death, in the degeneration of nucleus pulposus cells (NPCs). This research examines the protective role of 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], the active metabolite of Vitamin D (VD), in LIDD through the modulation of ferroptosis. The results indicate that 1,25(OH)₂D₃ significantly inhibits ferroptosis in NPCs through the reduction of lipid peroxidation, restoration of glutathione levels, and enhancement of antioxidant defenses. 1,25(OH)₂D₃ exerts its effects by activating the VD receptor (VDR) signaling pathway, which regulates important ferroptosis-associated molecules, including glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). The findings indicate the therapeutic potential of 1,25(OH)₂D₃ in alleviating LIDD, presenting a new strategy to inhibit ferroptosis and maintain intervertebral disc function.
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Registered trials
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