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August 14, 2025CytoJournalOpen Access

1α, 25-dihydroxyvitamin D3 attenuates tumor necrosis factor-α-induced endothelial cell injury by modulating the tumor necrosis factor-α/nuclear factor kappa-B pathway

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Authors

YXYangyang XiaNational Clinical ResearchSLSixiu LiuChinese Academy of SciencesQSQiuyuan ShaoNanjing Drum Tower Hospital

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Implication

In vitro analysis shows that 1α, 25(OH)2D3 reduces VCAM-1 and E-selectin in endothelial cells, implying its potential in treating cardiovascular diseases.

Key Points

  • 1α, 25(OH)2D3 significantly inhibits TNF-α-induced VCAM-1 and E-selectin expression in endothelial cells, indicating its protective effect.
  • The treatment reduced the activation of nuclear factor kappa-B signaling, lowering p65 expression and its binding to gene promoters.
  • ChIP assays confirmed that TNF-α enhanced p65 binding to VCAM-1 and E-selectin promoters, which was reversed by 1α, 25(OH)2D3.
  • The findings suggest that regulating the TNF-α/NF-κB pathway with vitamin D could benefit patients with cardiovascular diseases.

Cite This Study

Xia et al. (2025) studied this question.

synapsesocial.com/papers/68a363510a429f797332a5bfhttps://doi.org/10.25259/cytojournal_220_2024
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