Evidence map›Paper›PMID 22949934›Full record

ArticleInternational journal of clinical and experimental pathology2012

Telmisartan counteracts TGF-β1 induced epithelial-to-mesenchymal transition via PPAR-γ in human proximal tubule epithelial cells.

Yumin Chen, Qiong Luo, Zibo Xiong, Wei Liang, Li Chen, Zuying Xiong

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Maintenance of Kidney Metabolic Homeostasis by PPAR Gamma.International journal of molecular sciences · 2018
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Integrin β4 in EMT: an implication of renal diseases.International journal of clinical and experimental medicine · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Inhalation delivery of Telmisartan enhances intratumoral distribution of nanoparticles in lung cancer models.Journal of controlled release : official journal of the Controlled Release Society · 2013
    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

6 authors at 1 institution in 1 country.

Yumin ChenShenzhen Hospital, Health Science Center, Peking University, Shenzhen, PR China.
Qiong Luo
Zibo Xiong
Wei Liang
Li Chen
Zuying Xiong
Peking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic renal failure (CRF) mainly results from kidney fibrosis. Epithelial-to-mesenchymal transition (EMT) occurs in stressed tubular epithelial cells and contributes to renal fibrosis. Transforming growth factor-β1 (TGF-β1) has been shown to initiate and complete the whole EMT process. Peroxisome proliferators-activated receptor-γ (PPAR-γ) exerts anti-inflammatory, anti-fibrotic and vaculo-protective effects on different renal diseases. Telmisartan is a member of angiotensin II (Ang II) receptor blocker (ARB) family. Recent studies show that Telmisartan has a partial agonistic effect on PPAR-γ. Therefore, we tested the hypothesis that Telmisartan reverses the progression of induced EMT by TGF-β1 in cultured human renal proximal tubular epithelial (HK-2) cells. Cultured HK-2 cells were treated with TGF-β1 (3 ng/ml), a combination of TGF-β1 and Telmisartan (10-200 umol/L) and a combination of TGF-β1, Telmisartan and GW9662, a PPAR-γ antagonist for 48 hours. EMT was determined by quantitative real-time PCR analysis of E-cadherin (E-cad), Connective Tissue Growth Factor (CTGF) and PPAR-γ transcript expression and immunocytochemical analysis of E-cad, α-Smooth Muscle Actin (α-SMA) and PPAR-γ protein expression. TGF-β1 induced phenotypic EMT in cultured HK-2 cell line via significantly reduced E-cad expression and significantly increased CTGF, α-SMA expression in association with the loss of epithelial morphology. Telmisartan reversed all EMT markers in a dose-dependent manner which was inhibited by PPAR antagonist GW9662. In the present study, it was suggested that Telmisartan attenuated TGF-β1 induced EMT by agonistic activation of PPAR-γ.

Indexed as

Angiotensin II Type 1 Receptor BlockersBenzimidazolesBenzoatesCells, CulturedDrug AntagonismEpithelial CellsEpithelial-Mesenchymal TransitionHumansKidney Tubules, ProximalPPAR gammaTelmisartanTransforming Growth Factor beta1Angiotensin II Type 1 Receptor BlockersBenzimidazolesBenzoatesPPAR gammaTelmisartanTransforming Growth Factor beta1epithelial-to-mesenchymal transitionGW9662PPAR-γproximal tubular epithelial cellstelmisartanTGF-β1

Identifiers

PMID22949934
PMCPMC3430109
OpenAlexW1500983436

What Socratic 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 Socratic graph.