Evidence map›Paper›PMID 30684890›Full record

ArticleRedox biology2019

Adropin protects against liver injury in nonalcoholic steatohepatitis via the Nrf2 mediated antioxidant capacity.

Xu Chen, Hongliang Xue, Wanjun Fang, Ke Chen, Shen Chen, Wenqi Yang, Tianran Shen, Xuechen Chen, Peiwen Zhang, Wenhua Ling

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Adropin: A New Regulator of Testicular Function-What Do We Know So Far?International journal of molecular sciences · 2026
    Review
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14 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Xu ChenDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: cxu1024@gmail.com.
Hongliang XueDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: xuehongliang490@foxmail.com.
Wanjun FangDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: fangwj5@mail2.sysu.edu.cn.
Ke ChenDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: chenk67@mail2.sysu.edu.cn.
Shen ChenDepartment of Toxicology, School of Public Health, Sun Yat-sen University, 510080, PR China; Guangzhou Key Laboratory of Environmental Pollution and Health Risk Assessment, Guangzhou 510080, PR China. Electronic address: 834035345@qq.com.
Wenqi YangDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Laboratory Center for Sport Science and Medicine, Guangzhou Institute of Physical Education, Guangzhou 510080, PR China. Electronic address: yangwenqigw@126.com.
Tianran ShenDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: tianranshen@gmail.com.
Xuechen ChenDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: chxuech@mail2.sysu.edu.cn.
Peiwen ZhangDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: 313743920@qq.com.
Wenhua LingDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, PR China. Electronic address: lingwh@mail.sysu.edu.cn.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adropin, a secretory signal peptide, has shown beneficial effects on improving glucose homeostasis and dyslipidemia. However, whether this peptide affects nonalcoholic steatohepatitis (NASH) has remained unclear. In this study, the serum adropin levels, liver injury and oxidative stress were measured in diet-induced NASH mice. Adropin knock-out mice and palmitate treated primary hepatic cells were used to investigate the influence of adropin on liver injury. Our results show that serum adropin levels were decreased and negatively correlated with liver injury in NASH mice. Knockout of adropin significantly exacerbated hepatic steatosis, inflammatory responses and fibrosis in mice after either methionine-choline deficient diet (MCD) or western diet (WD) feeding. And the treatment with adropin bioactive peptides ameliorated NASH progression in mice. Adropin alleviated hepatocyte injury by upregulating the expression of Gclc, Gclm, and Gpx1 in a manner dependent on Nrf2 transcriptional activity and by increasing the glutathione (GSH) levels. And adropin significantly increased CBP expression and promoted its binding with Nrf2, which enhanced Nrf2 transcriptional activity. Furthermore, AAV8-mediated overexpression of hepatic Nrf2 expression functionally restored the liver injury induced by adropin-deficiency MCD-fed mice. These findings provide evidence that adropin activates Nrf2 signaling and plays a protective role in liver injury of NASH and therefore might represent a novel target for the prevention and treatment of NASH.

Indexed as

AnimalsAntioxidantsDisease Models, AnimalGene ExpressionHepatocytesIntercellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutNF-E2-Related Factor 2Non-alcoholic Fatty Liver DiseaseOxidation-ReductionOxidative StressProteinsTransduction, GeneticAntioxidantsEnho protein, mouseIntercellular Signaling Peptides and ProteinsNF-E2-Related Factor 2ProteinsGSHLipotoxicityNASHNrf2ROS

Identifiers

PMID30684890
PMCPMC6351233
OpenAlexW2905044900

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.