Evidence map›Paper›PMID 35560773›Full record

ReviewJournal of cellular and molecular medicine2022

Research progress of endothelial-mesenchymal transition in diabetic kidney disease.

Ying Chen, Hang Zou, Hongwei Lu, Hong Xiang, Shuhua Chen

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Lactate Metabolism and Protein Lactylation in Diabetic Kidney Disease: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  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

5 authors at 1 institution in 1 country.

Ying ChenDepartment of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, China.
Hang ZouDepartment of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, China.
Hongwei LuCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID 0000-0001-8005-142X
Hong XiangCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, China.
Shuhua ChenDepartment of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha, China.ORCID 0000-0003-2373-3402
Central South University · CN

Funding

Key Research and Development Program of Hunan Province of China 2019SK2041Key Research and Development Program of Hunan Province of China 2020SK2087National Natural Science Foundation of China 81870352National Natural Science Foundation of China 81970252
6 · The paper itself

Abstract

Renal fibrosis is an important pathological feature of diabetic kidney disease (DKD), manifested as tubular interstitial fibrosis, tubular atrophy, glomerulosclerosis and damage to the normal structure of the kidney. Renal fibrosis can eventually develop into renal failure. A better understanding of renal fibrosis in DKD is needed due to clinical limitations of current anti-fibrotic drugs in terms of effectiveness, cost-effectiveness and side effects. Fibrosis is characterized by local excessive deposition of extracellular matrix, which is derived from activated myofibroblasts to increase its production or specific tissue inhibitors of metalloproteinases to reduce its degradation. In recent years, endothelial-mesenchymal transition (EndMT) has gradually integrated into the pathogenesis of fibrosis. In animal models of diabetic kidney disease, it has been found that EndMT is involved in the formation of renal fibrosis and multiple signalling pathways such as TGF-β signalling pathway, Wnt signalling pathway and non-coding RNA network participate in the regulation of EndMT during fibrosis. Here, we mainly review EndMT regulation and targeted therapy of renal fibrosis in DKD.

Indexed as

Diabetes MellitusDiabetic NephropathiesAnimalsEndothelial CellsEpithelial-Mesenchymal TransitionFibrosisKidneyWnt Signaling Pathwaydiabetic kidney diseaseendothelial-mesenchymal transitionextracellular matrixrenal fibrosis

Identifiers

PMID35560773
PMCPMC9189345
OpenAlexW4280535581

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.