Evidence map›Paper›PMID 36601740›Full record

ArticleMolecular medicine reports2023

Role of SUMOylation of STAT1 in tubular epithelial‑mesenchymal transition induced by high glucose.

Cunyang Gu, Feng Gao, Shiqi Zhang, Lihua Kang, Wei Zhang, Xiaojuan Feng, Jinxi Liu, Yuexin Tian, Qun Wei, Yunxia Du and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Review
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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

13 authors at 2 institutions in 1 country.

Cunyang GuDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Feng GaoDepartment of Pathology, The Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
Shiqi ZhangDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Lihua KangDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Wei ZhangDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Xiaojuan FengDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Jinxi LiuDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Yuexin TianDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Qun WeiDepartment of Hospital Infection Control, Department of Public Health, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Yunxia DuDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Yujia XingDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Qingjuan LiuDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Shuxia LiuDepartment of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Hebei Medical University · CNHebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial fibrosis (TIF) is an important pathological change that occurs during the development of diabetic kidney disease. The epithelial‑mesenchymal transition (EMT) of renal tubular epithelial cells is a manifestation of TIF. STAT1, a member of the STAT family of transcription factors, can be modified by the small ubiquitin‑related modifier (SUMO), thus affecting the activity of STAT1. The present study investigated the role of STAT1 SUMOylation in high glucose‑induced tubular EMT by western blotting, immunocytochemistry, immunofluorescence, co‑immunoprecipitation and dual luciferase reporter analysis. The results indicated that in the process of high glucose‑induced EMT, STAT1 activation protected the cells from EMT. However, high glucose also increased the SUMOylation of STAT1, which prevented STAT1 from exerting an effective protective role by inhibiting its activity.

Indexed as

Epithelial-Mesenchymal TransitionSumoylationEpithelial CellsFibrosisGlucoseHumansSTAT1 Transcription FactorTranscription FactorsGlucoseSTAT1 protein, humanSTAT1 Transcription FactorTranscription Factorsepithelial‑mesenchymal transitionhigh glucoserenal tubular epithelial cellssmall ubiquitin‑related modifierSTAT1

Identifiers

PMID36601740
PMCPMC9835054
OpenAlexW4313397898

What Socratic 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 Socratic graph.