Evidence map›Paper›PMID 30483860›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2019

CCR2 and CCR5 promote diclofenac-induced hepatotoxicity in mice.

Zhanke He, Guoquan Wei, Na Li, Mengwei Niu, Shenhai Gong, Guangyan Wu, Teng Wang, Yong Jiang, Peng Chen

Erratum issuedAbstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Zhanke HeDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Guoquan WeiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Na LiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Mengwei NiuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Shenhai GongDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Guangyan WuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Teng WangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China.
Yong JiangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China. jiang48231@163.com.
Peng ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China. perchen@smu.edu.cn.
Southern Medical University · CN

Funding

Key Scientific and Technological Program of Guangzhou City 201607020016National Natural Science Foundation of China 81372030State Key Laboratory of Organ Failure Research 201804The Grant of NSFC-Guangdong Joint Foundation of China U1601225the Natural Science Funds for Distinguished Young Scholar of Guangdong province 2016A030306043
6 · The paper itself

Abstract

Liver injury, one of the major side effects of diclofenac (DIC), plagues thousands of patients who treated with it. Although involvements of metabolic factors, oxidative stress, and mitochondrial injury have been characterized, the exact immunomolecular mechanism of the hepatotoxicity of DIC still remains ambiguous. In this study, we investigated the role of chemokine receptors CCR2 and CCR5 in this progression. Ccr2, Ccr5, and Tnfr1/2-deficient mice, as well as wild type littermates, were administrated DIC or vehicle for 24 h, receptively. Hepatic expression of CCR2, CCR5, and their ligands were upregulated after DIC treatment. DIC-induced liver injury was augmented in Ccr2

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalChemical and Drug Induced Liver InjuryCytochrome P-450 Enzyme SystemDiclofenacGlucuronosyltransferaseLiverMaleMice, Inbred C57BLMice, KnockoutNeutrophilsReceptors, CCR2Receptors, CCR5Tumor Necrosis Factor-alphaAnti-Inflammatory Agents, Non-SteroidalCcr2 protein, mouseCCR5 protein, mouseCytochrome P-450 Enzyme SystemDiclofenacGlucuronosyltransferaseReceptors, CCR2Receptors, CCR5Tnf protein, mouseTumor Necrosis Factor-alphaAcute liver injuryCCR2CCR5DiclofenacNeutrophilsTNF-α

Identifiers

PMID30483860
OpenAlexW2902020872

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.