Evidence map›Paper›PMID 28949388›Full record

ArticleInternational journal of molecular medicine2017

MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner.

Xianggui Yang, Dongming Wu, Hongfei Du, Fang Nie, Xueli Pang, Ying Xu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. 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
1.5field-weighted citation impact, top 17% 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, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. MicroRNAs as Biomarkers for Nephrotic Syndrome.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. MicroRNA and Microvascular Complications of Diabetes.International journal of endocrinology · 2018
    Review
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

6 authors at 1 institution in 1 country.

Xianggui YangDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
Dongming WuDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
Hongfei DuDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
Fang NieDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
Xueli PangDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
Ying XuDepartment of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China.
First Affiliated Hospital of Chengdu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential (TRP) cation channels are essential for normal cellular physiology, and their abnormal expression may lead to a number of disorders, including podocytopathy. Therefore, it is crucial to understand the mechanisms underlying the regulation of TRP channels. In the present study, microRNA (miR)-135a was found to be upregulated in patients with focal segmental glomerulosclerosis and mice treated with adriamycin (ADR). In cultured podocytes, transforming growth factor (TGF)-β and ADR were found to promote miR‑135a expression. Conversely, TRP channel 1 (TRPC1) protein levels were markedly downregulated in podocytes from mice treated with ADR, as well as in cultured podocytes treated with ADR and TGF-β. Ectopic expression of miR-135a led to severe podocyte injury and disarray of the podocyte cytoskeleton, whereas podocyte-specific expression of TRPC1 was able to reverse the pathological effects of miR-135a in cultured podocytes. Moreover, using luciferase reporter assays and western blot analysis, TRPC1 was identified as a target gene of miR-135a. To the best of our knowledge, this is the first study to demonstrate the role of TRPC1 in the development of podocyte injury and disorders of the podocyte cytoskeleton, which may contribute to the development of novel therapeutics for podocyte injury-associated kidney diseases.

Indexed as

RNA Interference3' Untranslated RegionsAnimalsApoptosisCell LineDisease Models, AnimalGene Expression RegulationGlomerulosclerosis, Focal SegmentalHumansMiceMicroRNAsPodocytesTransfectionTRPC Cation Channels3' Untranslated RegionsMicroRNAsMIRN135 microRNA, humantransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID28949388
PMCPMC5627871
OpenAlexW2756885609

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.