Evidence map›Paper›PMID 30948420›Full record

ArticleEMBO molecular medicine2019

A KDM6A-KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction.

Chun-Liang Lin, Yung-Chien Hsu, Yu-Ting Huang, Ya-Hsueh Shih, Ching-Jen Wang, Wen-Chih Chiang, Pey-Jium Chang

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

  1. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Ethyl Acetate Fractions ofInternational journal of molecular sciences · 2024
    Article
  6. Review
  7. New Insights into the Role of KLF10 in Tissue Fibrosis.International journal of molecular sciences · 2024
    Review
  8. Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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 4 institutions in 1 country.

Chun-Liang LinDepartments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan.
Yung-Chien HsuDepartments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan.
Yu-Ting HuangDepartments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan.
Ya-Hsueh ShihDepartments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan.
Ching-Jen WangCenter for Shockwave Medicine and Tissue Engineering, Department of Medical Research, Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Wen-Chih ChiangDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Pey-Jium ChangDepartments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan peyjiumc@mail.cgu.edu.tw.ORCID 0000-0002-6492-0346
Chiayi Chang Gung Memorial Hospital · TWChang Gung University · TWKaohsiung Chang Gung Memorial Hospital · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up-regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte-specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes-induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both

Indexed as

Feedback, PhysiologicalAnimalsBase SequenceCell Line, TransformedDiabetic NephropathiesDown-RegulationEarly Growth Response Transcription FactorsEpigenesis, GeneticExosomesHistone DemethylasesHumansKidneyKruppel-Like Transcription FactorsMaleMembrane ProteinsMice, Inbred C57BLEarly Growth Response Transcription FactorsHistone DemethylasesKDM6A protein, humanKLF10 protein, humanKLF10 protein, mouseKruppel-Like Transcription FactorsMembrane ProteinsnephrinUtx protein, mousediabetic nephropathyepigeneticsKDM6AKLF10podocyte dysfunction

Identifiers

PMID30948420
PMCPMC6505577
OpenAlexW2933026945

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.