ArticleBMC gastroenterology2025
Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
backgroundThe increased apoptosis of bile duct epithelial cells (BECs) due to some damage factors is considered the initiating factor in the occurrence and progression of biliary atresia (BA). Vitamin D receptor (VDR) is thought to play a crucial role in maintaining the intrinsic immune balance and integrity of bile duct epithelial cells (BECs). To investigate the role of VDRs in the pathogenesis and progression of BA using in vitro and in vivo models. MATERIALS AND
methodsThe VDR expression levels in intrahepatic bile duct epithelial cells (IBDECs) in pediatric patients with BA were examined using immunohistochemical analysis. The correlation of the VDR levels with the incidence of refractory cholangitis after Kasai portoenterostomy (KPE) and the autologous liver survival time was analyzed. The levels of genes and proteins involved in related pathways were examined using quantitative real-time polymerase chain reaction and western blotting, respectively. The secretory levels of inflammatory factors were analyzed using enzyme-linked immunosorbent assay. A BA mouse model was established through the intraperitoneal sequential injection of rhesus rotavirus (RRV). The role of VDR in the pathogenesis and progression of BA was examined using in vitro and in vivo models. Retrospective analysis of patients with BA to examine the therapeutic efficacy of VDR activators on BA.
results15 pediatric BA patients exhibiting VDR downregulation in IBDECs showed a higher incidence of refractory cholangitis after Kasai portoenterostomy (p = 0.037) and a lower native liver survival time compare to 23 BA patients without VDR downregulation (p = 0.032). 1,25-VD3 inhibited the degree of autophagy induction in HIBECs by poly(I: C) (p < 0.05), mitigated poly(I: C)-induced BEC damage and apoptosis by inhibiting autophagy (p < 0.05). 1,25-VD3 significantly suppressed the poly(I: C)-induced downregulation of SRC (p < 0.05) and ERK1/2 phosphorylation (p < 0.05). 1,25-VD3 exert a protective effect against RRV-induced BEC damage by inhibiting autophagy in BA mouse model. The incidence of cholangitis and the native liver survival time after surgery in the calcitriol-treated group was significantly lower than that in the control group. (p = 0.033, p = 0.035, respectively).
conclusionsVDR activator mitigated dsRNA-induced BEC damage and apoptosis by inhibiting autophagy in vitro and in vivo. The 1,25-VD3/VDR/Src axis alleviated poly(I: C)-induced HIBEC damage and apoptosis through the PLA2/PKC/ERK pathway.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.