Evidence map›Paper›PMID 25056456›Full record

ArticleScientific reports2014

Antifibrotic effects of KS370G, a caffeamide derivative, in renal ischemia-reperfusion injured mice and renal tubular epithelial cells.

Sung-Ting Chuang, Yueh-Hsiung Kuo, Ming-Jai Su

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. 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
1.8field-weighted citation impact, top 17% 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, 19 citations in OpenAlex.

  1. International journal of molecular sciences · 2022
    Article
  2. Article
  3. Biochemistry and biophysics reports · 2021
    Article
  4. Article
  5. Article
  6. A Nucleoside/Nucleobase-Rich Extract fromMolecules (Basel, Switzerland) · 2019
    Article
  7. Caffeic Acid Modulates miR-636 Expression in Diabetic Nephropathy Rats.Indian journal of clinical biochemistry : IJCB · 2019
    Article
  8. Article
  9. Cardioprotection of CAPE-oNORedox biology · 2018
    Article
  10. Review
  11. CAPE-Oncotarget · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. 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

3 authors at 2 institutions in 1 country.

Sung-Ting ChuangInstitute of Pharmacology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
Yueh-Hsiung Kuo1] Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 40402, Taiwan [2] Department of Biotechnology, Asia University, Taichung 41354, Taiwan.
Ming-Jai SuInstitute of Pharmacology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.
National Taiwan University · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that renal tubulointerstitial fibrosis is a main cause of end-stage renal disease. Clinically, there are no beneficial treatments that can effectively reverse the progressive loss of renal functions. Caffeic acid phenethyl ester is a natural phenolic antifibrotic agent, but rapid decomposition by an esterase leads to its low bioavailability. In this study, we evaluated the effects of KS370G, a caffeic acid phenylethyl amide, on murine renal fibrosis induced by unilateral renal ischemia-reperfusion injury (IRI) and in TGF-β₁ stimulated renal tubular epithelial cells (NRK52E and HK-2). In the animal model, renal fibrosis was evaluated at 14 days post-operation. Immediately following the operation, KS370G (10 mg/kg) was administered by oral gavage once a day. Our results show that KS370G markedly attenuates collagen deposition and inhibits an IRI-induced increase of fibronectin, vimentin, α-SMA and TGF-β₁ expression and plasma TGF-β₁ levels in the mouse kidney. Furthermore, KS370G reverses TGF-β1-induced downregulation of E-cadherin and upregulation of α-SMA and also decreases the expression of fibronectin, collagen I and PAI-1 and inhibits TGF-β₁-induced phosphorylation of Smad2/3. These findings show the beneficial effects of KS370G on renal fibrosis in vivo and in vitro with the possible mechanism being the inhibition of the Smad2/3 signaling pathway.

Indexed as

AnimalsCaffeic AcidsCdh1 ProteinsCell LineCollagenEpithelial CellsEpithelial-Mesenchymal TransitionFibronectinsFibrosisHumansIschemiaKidney DiseasesKidney TubulesMaleMice, Inbred ICRPhosphorylationCaffeic AcidsCdh1 ProteinsCollagenFibronectinsFzr1 protein, mouseKS370GSerpin E2Serpine2 protein, mouseSmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseTgfb1 protein, mouseTransforming Growth Factor beta1Vimentin

Identifiers

PMID25056456
PMCPMC4108915
OpenAlexW2034637868

What OpenQuestion holds

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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.