Evidence map›Paper›PMID 31467925›Full record

ArticleJournal of diabetes research2019

Nrf2-Heme Oxygenase-1 Attenuates High-Glucose-Induced Epithelial-to-Mesenchymal Transition of Renal Tubule Cells by Inhibiting ROS-Mediated PI3K/Akt/GSK-3

Jong Ho Shin, Kyeong Min Kim, Jin Uk Jeong, Jae Min Shin, Ju Hyung Kang, Kitae Bang, Joo-Heon Kim

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.5field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Deciphering the impact ofGenes & diseases · 2026
    Article
  4. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  5. Urinary biomarkers of diabetic kidney disease.World journal of diabetes · 2026
    Review
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  8. Review
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  18. Article
  19. Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022
    Review
  20. 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.

Jong Ho ShinDivision of Nephrology, Eulji University College of Medicine, Daejeon, Republic of Korea.
Kyeong Min KimDivision of Nephrology, Eulji University College of Medicine, Daejeon, Republic of Korea.
Jin Uk JeongDivision of Nephrology, Eulji University College of Medicine, Daejeon, Republic of Korea.
Jae Min ShinDivision of Pathology, Eulji University College of Medicine, Daejeon, Republic of Korea.
Ju Hyung KangDivision of Pediatrics, Eulji University College of Medicine, Daejeon, Republic of Korea.
Kitae BangDivision of Nephrology, Eulji University College of Medicine, Daejeon, Republic of Korea.ORCID https://orcid.org/0000-0002-8469-2010
Joo-Heon KimDivision of Pathology, Eulji University College of Medicine, Daejeon, Republic of Korea.ORCID https://orcid.org/0000-0001-7592-0985
Eulji University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-to-mesenchymal transition (EMT) is thought to play a significant role in the advancement to chronic kidney disease and contributes to the deposition of extracellular matrix proteins and renal fibrosis relating to diabetic nephropathy.

methodWe studied the effect of Nrf2-HO-1 signaling on high-glucose- (HG-) induced EMT in normal human tubular epithelial cells, that is, HK2 cells. In short, we treated HK2 cells with HG and sulforaphane (SFN) as an Nrf2 activator. EMT was evaluated by the expression activity of the epithelial marker E-cadherin and mesenchymal markers such as vimentin and fibronectin.

resultsExposure of HK2 cells to HG (60 mM) activated the expression of vimentin and fibronectin but decreased E-cadherin. Treatment of HK2 cells with SFN caused HG-induced attenuation in EMT markers with activated Nrf2-HO-1. We found that SFN decreased HG-induced production of reactive oxygen species (ROS), phosphorylation of PI3K/Akt at serine 473, and inhibitory phosphorylation of serine/threonine kinase glycogen synthase kinase-3

conclusionThe present study suggests that Nrf2-HO-1 signaling has an inhibitory role in the regulation of EMT through the modulation of ROS-mediated PI3K/Akt/GSK-3

Indexed as

Cells, CulturedDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionGlucoseGlycogen Synthase Kinase 3 betaHEK293 CellsHeme Oxygenase-1HumansKidney TubulesNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionGlucoseGlycogen Synthase Kinase 3 betaHeme Oxygenase-1HMOX1 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID31467925
PMCPMC6701369
OpenAlexW2966372139

What OpenQuestion holds

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LicenceCC BY
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.