Evidence map›Paper›PMID 26884948›Full record

ArticleInternational journal of clinical and experimental medicine2015

KLF15 suppresses cell proliferation and extracellular matrix expression in mesangial cells under high glucose.

Jun Zhang, Hong-Bin Zhong, Ying Lin, Wang Yao, Ji-Yi Huang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Sildenafil suppresses the activation of hypertrophic scar fibroblasts by promoting the KLF15-mediated inhibition ofThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  4. Review
  5. Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Signaling Pathways Involved in Diabetic Renal Fibrosis.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Krüppel-like Factor 15: A Potential Therapeutic Target For Kidney Disease.International journal of biological sciences · 2019
    Review
  12. Article
  13. Article
  14. 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.

Jun ZhangDepartment of Nephrology, The First Affiliated Hospital of Xiamen University, Tongmin Branch Court Xiamen 361000, China.
Hong-Bin ZhongDepartment of Nephrology, The First Affiliated Hospital of Xiamen University, Tongmin Branch Court Xiamen 361000, China.
Ying LinDepartment of Nephrology, The First Affiliated Hospital of Xiamen University, Tongmin Branch Court Xiamen 361000, China.
Wang YaoMedical College Xiamen University Xiamen 361102, China.
Ji-Yi HuangDepartment of Nephrology, The First Affiliated Hospital of Xiamen University, Tongmin Branch Court Xiamen 361000, China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess mesangial extracellular matrix (ECM) and mesangial cell (MC) proliferation is the major pathologic feature of diabetic nephropathy. Kruppel-like factor 15 (KLF15) is a member of the KLF transcription factor family that plays a critical role in regulating renal fibrosis. However, the role of KLF15 in diabetic nephropathy remains poorly understood. This study was conducted to explore the role of KLF15 in the development and progress of diabetic nephropathy in high glucose (HG)-stimulated human MCs. Here, we found down-regulated expression of KLF15 in MCs induced by HG. Overexpression of KLF15 significantly inhibited MCs proliferation and ECM production induced by HG. Moreover, overexpression of KLF15 inhibited HG-induced ERK1/2 phosphorylation in MCs. In summary, our data demonstrate that KLF15 can suppress HG-induced cell proliferation and ECM protein fibronectin expression in human MCs via ERK1/2 MAPK signaling. The results provide evidence that KLF15 might be a potential molecular target for the treatment of diabetic nephropathy.

Indexed as

diabetic nephropathyextracellular matrix (ECMKruppel-like factor 15 (KLF15)mesangial cells (MCs)

Identifiers

PMID26884948
PMCPMC4723793
OpenAlexW2413526751

What OpenQuestion holds

Textmetadata
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.