ArticleCytoJournal2025
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.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Cardiovascular (CV) diseases remain the leading cause of death in modern societies, with endothelial dysfunction being the common pathology of CV diseases with various etiologies. Therefore, effectively regulating the function of endothelial cells is considered the key to the future treatment of various CV diseases. Low levels of vitamin D and its analogs have been shown to be associated with endothelial dysfunction in various diseases. However, the underlying mechanism remains unknown. Here, we conducted an Material and Methods: Human umbilical vein endothelial cells were cultured and treated according to the experimental requirements. Western blotting and reverse transcription polymerase chain reaction were used to evaluate the expression of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. Chromatin immunoprecipitation (ChIP) assays, immunofluorescence, Western blotting, and coimmunoprecipitation were used to assess the effects of 1α, 25(OH)2D3 on nuclear factor kappa-B (NF-κB) signaling. Results: 1α, 25(OH)2D3 inhibited VCAM-1 and E-selectin mRNA and protein expression after tumor necrosis factor-α (TNF-α) stimulation. Moreover, 1α, 25(OH)2D3 affected TNF-α-induced IκBα phosphorylation and p65 NF-κB activation, leading to the inhibition of p65 expression. A ChIP assay revealed that TNF-α increased p65 binding to the promoters of VCAM-1 and E-selectin, which was suppressed by 1α, 25(OH)2D3. These effects were abrogated by a specific vitamin D receptor siRNA (VDR-siRNA). Coimmunoprecipitation revealed that 1α, 25(OH)2D3 induced increased binding of the vitamin D receptor to p65, which inhibited the ability of p65 to bind to target gene promoters. Conclusion: 1α, 25(OH)2D3 regulates adhesion molecule expression in endothelial cells through the TNF-α/NF-κB pathway, laying the foundation for the clinical application of 1α, 25(OH)2D3 in the treatment of CV diseases.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.