Evidence map›Paper›PMID 31863364›Full record

ArticleJournal of nephrology2020

MicroRNA-21-5p participates in IgA nephropathy by driving T helper cell polarization.

Bo-Yang Xu, Si-Jun Meng, Su-Fang Shi, Li-Jun Liu, Ji-Cheng Lv, Li Zhu, Hong Zhang

Abstract read
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In one paragraph

Article in Journal of nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. An Update on the Genetics of IgA Nephropathy.Journal of clinical medicine · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. MicroRNAs in IgA nephropathy.Renal failure · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. T lymphocytes in IgA nephropathy.Experimental and therapeutic medicine · 2020
    Article
  19. 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.

Bo-Yang XuRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Si-Jun MengRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Su-Fang ShiRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Li-Jun LiuRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Ji-Cheng LvRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China.
Li ZhuRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China. funnyzhuli@bjmu.edu.cn.
Hong ZhangRenal Division, Department of Medicine, Peking University First Hospital, Beijing, 100034, China. hongzh@bjmu.edu.cn.

Funding

National Key Research and Development Program of China 2016YFC0904102National Science Foundation for Excellent Young Scholars 81922013National Science Foundation of China 81670638National Science Foundation of China 81970598Natural Science Foundation of Beijing, China 7202206Training Program of the Major Research Plan of the National Natural Science Foundation of China 91642120
6 · The paper itself

Abstract

backgroundPrevious studies have revealed abnormal lymphocyte subsets in IgA nephropathy (IgAN). Some microRNAs have been reported to influence T helper differentiation. Here, we explored the underlying mechanism regarding how miRNAs regulate lymphocyte subsets in IgAN.

methodsFirst, miRNA and mRNA profiles in PBMCs from IgAN patients and controls were obtained by next-generation sequencing and gene expression array. The target miRNAs and mRNAs were identified through combined analysis. Then, in an independent population, we detected the expression of target miRNA in CD3

resultsIn total, 22 differentially expressed miRNAs were identified between IgAN patients and controls. Among them, microRNA-21-5p (miR-21) showed the highest expression, and SPRY1, SPRY2, and FASLG were chosen as miR-21 target genes. Then, we confirmed elevated miR-21 levels in CD3

conclusionsOur results suggested that in IgAN, the upregulated miR-21 expression in T lymphocytes inhibited SPRY1 expression and thereby induced Th17 polarization, which might influence the characteristic feature of IgA1 overproduction in IgAN patients.

Indexed as

Glomerulonephritis, IGAMicroRNAsHumansImmunoglobulin AIntracellular Signaling Peptides and ProteinsMembrane ProteinsRNA, MessengerT-Lymphocytes, Helper-InducerImmunoglobulin AIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN21 microRNA, humanRNA, MessengerSPRY2 protein, humanIgA nephropathyMicroRNA-21-5pSPRY1Th17

Identifiers

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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.