Evidence map›Paper›PMID 28680529›Full record

ArticleOxidative medicine and cellular longevity2017

miR-382 Contributes to Renal Tubulointerstitial Fibrosis by Downregulating HSPD1.

Yi Fang, Ting Xie, Ning Xue, Qing Kuang, Zheng Wei, Mingyu Liang, Xiaoqiang Ding

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. 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
2.0field-weighted citation impact, top 13% 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, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023
    Review
  5. MicroRNA-382 Promotes M2-Like MacrophageFrontiers in immunology · 2022
    Article
  6. Review
  7. MicroRNA-302b mitigates renal fibrosis via inhibiting TGF-β/Smad pathway activation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. 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 2 institutions in 2 countries.

Yi FangDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-8675-4513
Ting XieDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Ning XueDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Qing KuangDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Zheng WeiDepartment of Hematology, Zhongshan Hospital, Fudan University, Shanghai, China.
Mingyu LiangDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.ORCID 0000-0002-6970-989X
Xiaoqiang DingDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-5269-2868
Sun Yat-sen University · CNMedical College of Wisconsin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Redox imbalance plays an important role in the pathogenesis of CKD progression. Previously, we demonstrated that microRNA-382 (miR-382) contributed to TGF-

Indexed as

AnimalsCell LineChaperonin 60Down-RegulationFibrosisGlomerulonephritis, IGAHumansKidney TubulesMaleMiceMice, Inbred ICRMicroRNAsMitochondrial ProteinsTransfectionChaperonin 60HSPD1 protein, humanHspd1 protein, mousemicroRNA 382, mouseMicroRNAsMIRN382 microRNA, humanMitochondrial Proteins

Identifiers

PMID28680529
PMCPMC5478870
OpenAlexW2622233400

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.