Evidence map›Paper›PMID 33942213›Full record

ArticleInternational urology and nephrology2021

Vitamin D protects glomerular mesangial cells from high glucose-induced injury by repressing JAK/STAT signaling.

Yiya Yang, Yuting Lei, Yumei Liang, Shuangshuang Fu, Congjun Yang, Kanghan Liu, Yinyin Chen

Open access · hybridAbstract read
In one paragraph

Article in International urology and nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Insights into the mechanisms of angiogenesis in hepatoblastoma.Frontiers in cell and developmental biology · 2025
    Review
  7. Article
  8. Inflammation in glomerular diseases.Frontiers in immunology · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023
    Review
  15. The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy.International journal of nephrology and renovascular disease · 2023
    Review
  16. The Role of Vitamin D in Diabetic Nephropathy: A Translational Approach.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
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.

Yiya YangDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Yuting LeiDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Yumei LiangDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Shuangshuang FuDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Congjun YangDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Kanghan LiuDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China.
Yinyin ChenDepartment of Nephrology and Laboratory of Kidney Disease, Changsha Clinical Research Center for Kidney DiseaseHunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, Hunan Normal University, 61#, Jiefang West Road, Changsha, 410005, Hunan Province, People's Republic of China. chenchenyinyin1212@163.com.ORCID http://orcid.org/0000-0002-7454-2596
Hunan Normal University · CN

Funding

Hunan Provincial Science and Technology Department 2018SK50701
6 · The paper itself

Abstract

aimHigh glucose (HG) induces the production of transforming growth factor (TGF)-β and reactive oxygen species, which further activates JAK/STAT signaling and promotes the synthesis of matrix proteins, contributes to the pathophysiological processes of diabetic nephropathy. This study aims to investigate the protection role of vitamin D (VD) in the kidney in high glucose condition.

methodsRat glomerular mesangial cells were cultured in high glucose medium, with or without VD or VD receptor (VDR) siRNAs treatment. The levels of TGF-β and fibronectin were detected by qRT-PCR, immunoblotting and enzyme-linked immunosorbent assay (ELISA). The levels of phosphorylated JAK2, STAT1 and STAT3, and JAK/STAT signaling downstream genes were examined by immunoblotting and qRT-PCR.

resultsIn rat glomerular mesangial cells, VD treatment can repress the tyrosine phosphorylation of JAK2, STAT1 and STAT3. VD inhibited TGF-β and fibronectin expression which was rescued by vitamin d receptor (VDR) siRNA and STATs inhibitor perficitinib. The JAK/STAT signaling downstream protein coding genes including SOCS1, SOCS3 and type IV collagen were repressed by VD. Meanwhile, the expression of non-coding RNAs such as miR-181a, miR-181b, was repressed by VD, and the expression of miR-34a and Let-7b was upregulated by VD.

conclusionVitamin D (VD) treatment inhibits the function of HG on fibronectin production through regulating JAK/STAT pathway. These results provide direct evidences that VD protects glomerular mesangial cells from high glucose-induced injury through repressing JAK/STAT signaling, which has the potential for clinical DN treatment.

Indexed as

AnimalsCells, CulturedGlucoseJanus Kinase 2MaleMesangial CellsRatsRats, Sprague-DawleySignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorVitamin DVitaminsGlucoseJak2 protein, ratJanus Kinase 2Stat1 protein, ratSTAT1 Transcription FactorStat3 protein, ratSTAT3 Transcription FactorVitamin DVitaminsGlumerular cellHigh glucoseJAK/STATReactive oxygen speciesVitamin D

Identifiers

PMID33942213
PMCPMC8144147
OpenAlexW3157938815

What OpenQuestion holds

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LicenceCC BY
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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.