Evidence map›Paper›PMID 34615940›Full record

ArticleScientific reports2021

Effect and mechanism of vitamin D activation disorder on liver fibrosis in biliary atresia.

Song Sun, Menghua Xu, Peijun Zhuang, Gong Chen, Kuiran Dong, Rui Dong, Shan Zheng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. The effects of low-fat dairy products fortified with 1500 IU vitamin DJournal of health, population, and nutrition · 2023
    Trial
  2. The bile acid-gut microbiota-vitamin D axis: new insights into biliary atresia.Frontiers in cellular and infection microbiology · 2026
    Review
  3. Review
  4. Article
  5. Manganese Deficiency and MnInternational journal of molecular sciences · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Song Sun *Surgical Department, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China.
Menghua Xu *The Center of Laboratory Medicine, Children's Hospital of Fudan University, Shanghai, 201102, China.
Peijun Zhuang *Anesthesiology Department, Children's Hospital of Fudan University, Shanghai, 201102, China.
Gong ChenSurgical Department, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China.
Kuiran DongSurgical Department, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China.
Rui DongSurgical Department, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China. dongrui_1982@126.com.
Shan ZhengSurgical Department, Children's Hospital of Fudan University, 399 Wanyuan Road, Shanghai, 201102, China. szheng@shmu.edu.cn.
Children's Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the mechanism of 25 hydroxyvitamin D (25(OH)D) deficiency in children with biliary atresia (BA) and its effect on liver fibrosis. The serum vitamin D and 25(OH)D, and expression of 25 hydroxylase (CYP2R1 and CYP27A1) in the liver of BA patients were detected and compared with those in the control group. We investigated the effect of differential expression of CYP2R1 in hepatocytes on the expression of genes related to liver fibrosis in primary hepatic stellate cells (HSCs) of BA and animal models of cholestasis. The ratio of 25(OH)D/vitamin D in the BA group was significantly lower than that in the control group. The mRNA and protein expression of CYP2R1 and CYP27A1 in liver tissue of the BA group was significantly lower than that in the control group. Exogenous active vitamin D (calcitriol) inhibited the proliferation and migration of primary HSCs isolated from BA patients, and reduced the expression of fibrosis-related genes in vitro. Downregulation of expression of CYP2R1 in hepatocytes increased expression of transforming growth factor (TGF)-β1, collagen (Col)-1α1 and tissue inhibitor of metalloproteinase (TIMP)-1, and decreased the expression of matrix metalloproteinase (MMP)-2 in cocultured primary HSCs of BA. Upregulation of expression of CYP2R1 in mice with bile duct ligation significantly increased the level of 25(OH)D, decreased the expression of TGF-β1, Col-1α1 and TIMP-1, and increased the expression of MMP-2. Children with BA have impaired vitamin D activation due to CYP2R1 deficiency. The dysactivation of vitamin D can promote the proliferation and activation of HSCs and participate in the development of hepatic fibrosis in BA.

Indexed as

BiomarkersDisease SusceptibilityBiliary AtresiaCell MovementCell ProliferationCells, CulturedCholestanetriol 26-MonooxygenaseCytochrome P450 Family 2FemaleGene ExpressionHepatic Stellate CellsHepatocytesHumansImmunohistochemistryInfantInfant, NewbornBiomarkersCholestanetriol 26-MonooxygenaseCYP27A1 protein, humanCYP2R1 protein, humanCytochrome P450 Family 2Vitamin D

Identifiers

PMID34615940
PMCPMC8494743
OpenAlexW3203685200

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.