Evidence map›Paper›PMID 26942460›Full record

ArticleOncotarget2016

C/EBP homologous protein (CHOP) deficiency ameliorates renal fibrosis in unilateral ureteral obstructive kidney disease.

Shing-Hwa Liu, Cheng-Tien Wu, Kuo-How Huang, Ching-Chia Wang, Siao-Syun Guan, Li-Ping Chen, Chih-Kang Chiang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
3.2field-weighted citation impact, top 9% 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, 35 citations in OpenAlex.

  1. Review
  2. The Role of C/EBP-Homologous Protein in Idiopathic Inflammatory Myopathies.Journal of cellular and molecular medicine · 2025
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  18. Endoplasmic Reticulum Stress-Induced CHOP Inhibits PGC-1α and Causes Mitochondrial Dysfunction in Diabetic Embryopathy.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
  19. Review
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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

7 authors at 3 institutions in 1 country.

Shing-Hwa LiuInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Cheng-Tien WuInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Kuo-How HuangDepartment of Urology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ching-Chia WangDepartment of Pediatrics, College of Medicine, National Taiwan University & Hospital, Taipei, Taiwan.
Siao-Syun GuanInstitute of Nuclear Energy Research, Atomic Energy Council, Taoyuan, Taiwan.
Li-Ping ChenDepartment of Dentistry, Taipei Chang Gang Memorial Hospital, Chang Gang University, Taipei, Taiwan.
Chih-Kang ChiangInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University Hospital · TWNational Taiwan University · TWInstitute of Nuclear Energy Research · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubulointerstitial fibrosis is an important pathogenic feature in chronic kidney disease and end-stage renal disease, regardless of the initiating insults. A recent study has shown that CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) is involved in acute ischemia/reperfusion-related acute kidney injury through oxidative stress induction. However, the influence of CHOP on chronic kidney disease-correlated renal fibrosis remains unclear. Here, we investigated the role of CHOP in unilateral ureteral obstruction (UUO)-induced experimental chronic tubulointerstital fibrosis. The CHOP knockout and wild type mice with or without UUO were used. The results showed that the increased expressions of renal fibrosis markers collagen I, fibronectin, α-smooth muscle actin, and plasminogen activator inhibitor-1 in the kidneys of UUO-treated wild type mice were dramatically attenuated in the kidneys of UUO-treated CHOP knockout mice. CHOP deficiency could also ameliorate lipid peroxidation and endogenous antioxidant enzymes depletion, tubular apoptosis, and inflammatory cells infiltration in the UUO kidneys. These results suggest that CHOP deficiency not only attenuates apoptotic death and oxidative stress in experimental renal fibrosis, but also reduces local inflammation, leading to diminish UUO-induced renal fibrosis. Our findings support that CHOP may be an important signaling molecule in the progression of chronic kidney disease.

Indexed as

AnimalsFibrosisMiceMice, KnockoutRenal Insufficiency, ChronicTranscription Factor CHOPUreteral ObstructionDdit3 protein, mouseTranscription Factor CHOPCHOPoxidative stressrenal fibrosisunilateral ureteral obstruction

Identifiers

PMID26942460
PMCPMC5008332
OpenAlexW2308491720

What OpenQuestion holds

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Registered trials

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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.