Evidence map›Paper›PMID 24475141›Full record

ArticlePloS one2014

Farnesoid X receptor ligand prevents cisplatin-induced kidney injury by enhancing small heterodimer partner.

Eun Hui Bae, Hong Sang Choi, Soo Yeon Joo, In Jin Kim, Chang Seong Kim, Joon Seok Choi, Seong Kwon Ma, Jongun Lee, Soo Wan Kim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  8. Role of FXR in Renal Physiology and Kidney Diseases.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Knockout of farnesoid X receptor gene aggravates cisplatin-induced kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Update on FXR Biology: Promising Therapeutic Target?International journal of molecular sciences · 2018
    Review
  18. Article
  19. Article
  20. Review
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

9 authors at 1 institution in 1 country.

Eun Hui BaeDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Hong Sang ChoiDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Soo Yeon JooDepartment of Physiology, Chonnam National University Medical School, Gwangju, Korea.
In Jin KimDepartment of Physiology, Chonnam National University Medical School, Gwangju, Korea.
Chang Seong KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Joon Seok ChoiDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Seong Kwon MaDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Jongun LeeDepartment of Physiology, Chonnam National University Medical School, Gwangju, Korea.
Soo Wan KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Chonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The farnesoid X receptor (FXR) is mainly expressed in liver, intestine and kidney. We investigated whether 6-ethyl chenodeoxycholic acid (6ECDCA), a semisynthetic derivative of chenodeoxycholic aicd (CDCA, an FXR ligand), protects against kidney injury and modulates small heterodimer partner (SHP) in cisplatin-induced kidney injury. Cisplatin inhibited SHP protein expression in the kidney of cisplatin-treated mice and human proximal tubular (HK2) cells; this effect was counteracted by FXR ligand. Hematoxylin and eosin staining revealed the presence of tubular casts, obstructions and dilatations in cisplatin-induced kidney injury, which was attenuated by FXR ligand. FXR ligand also attenuated protein expression of transforming growth factor-β1 (TGF-β1), Smad signaling, and the epithelial-to-mesenchymal transition process, inflammatory markers and cytokines, and apoptotic markers in cisplatin-treated mice. Cisplatin induced NF-κB activation in HK2 cell; this effect was attenuated by pretreatment with FXR ligand. In SHP knockdown by small interfering RNA, cisplatin-induced activation of TGF-β1, p-JNK and Bax/Bcl-2 ratio was not attenuated, while SHP overexpression and FXR ligand inhibited expression of these proteins in cisplatin-pretreated HK2 cells. In conclusion, FXR ligand, 6ECDCA prevents cisplatin-induced kidney injury, the underlying mechanism of which may be associated with anti-fibrotic, anti-inflammatory, and anti-apoptotic effects through SHP induction.

Indexed as

Acute Kidney InjuryAnalysis of VarianceAnimalsChenodeoxycholic AcidCisplatinDNA PrimersEpithelial-Mesenchymal TransitionImmunoblottingImmunoenzyme TechniquesIn Situ Nick-End LabelingMaleMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearChenodeoxycholic AcidCisplatinDNA Primersnuclear receptor subfamily 0, group B, member 2obeticholic acidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, Small InterferingTransforming Growth Factor beta1

Identifiers

PMID24475141
PMCPMC3903546
OpenAlexW2082583283

What OpenQuestion holds

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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.