Evidence map›Paper›PMID 32375062›Full record

ArticleCell metabolism2020

Low-Dose Sorafenib Acts as a Mitochondrial Uncoupler and Ameliorates Nonalcoholic Steatohepatitis.

Chongshu Jian, Jiajun Fu, Xu Cheng, Li-Jun Shen, Yan-Xiao Ji, Xiaoming Wang, Shan Pan, Han Tian, Song Tian, Rufang Liao and 9 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2020. 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 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
13.8field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 167 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 5 institutions in 2 countries.

Chongshu JianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Jiajun FuInstitute of Model Animal of Wuhan University, Wuhan 430071, China; Medical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Xu ChengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Li-Jun ShenDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Yan-Xiao JiInstitute of Model Animal of Wuhan University, Wuhan 430071, China; Medical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Xiaoming WangInstitute of Model Animal of Wuhan University, Wuhan 430071, China; School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Shan PanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Han TianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Song TianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Rufang LiaoDepartment of Radiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Kehan SongDepartment of Orthopaedic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Hai-Ping WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Xin ZhangInstitute of Model Animal of Wuhan University, Wuhan 430071, China; College of Life Sciences, Wuhan University, Wuhan 430072, China.
Yibin WangDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Zan HuangCollege of Life Sciences, Wuhan University, Wuhan 430072, China.
Zhi-Gang SheDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China.
Xiao-Jing ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China. Electronic address: zhangxjing@whu.edu.cn.
Lihua ZhuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China. Electronic address: zhulh@whu.edu.cn.
Hongliang LiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Model Animal of Wuhan University, Wuhan 430071, China; Medical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China; School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China. Electronic address: lihl@whu.edu.cn.
Wuhan University · CNRenmin Hospital of Wuhan University · CNHuazhong University of Science and Technology · CNUniversity of California, Los Angeles · USZhongnan Hospital of Wuhan University · CN

Funding

BCAA Catabolic Defect in HF: Novel Mechanism and Therapeutic TargetR01HL140116 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, ZHAOPING · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL140116
6 · The paper itself

Abstract

Nonalcoholic steatohepatitis (NASH) is becoming one of the leading causes of hepatocellular carcinoma (HCC). Sorafenib is the only first-line therapy for advanced HCC despite its serious adverse effects. Here, we report that at an equivalent of approximately one-tenth the clinical dose for HCC, sorafenib treatment effectively prevents the progression of NASH in both mice and monkeys without any observed significant adverse events. Mechanistically, sorafenib's benefit in NASH is independent of its canonical kinase targets in HCC, but involves the induction of mild mitochondrial uncoupling and subsequent activation of AMP-activated protein kinase (AMPK). Collectively, our findings demonstrate a previously unappreciated therapeutic effect and signaling mechanism of low-dose sorafenib treatment in NASH. We envision that this new therapeutic strategy for NASH has the potential to translate into a beneficial anti-NASH therapy with fewer adverse events than is observed in the drug's current use in HCC.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, HepatocellularCell LineDose-Response Relationship, DrugHumansLiver NeoplasmsMaleMiceMice, Inbred C57BLMitochondriaNon-alcoholic Fatty Liver DiseaseSorafenibAntineoplastic AgentsSorafenibAMP–activated protein kinase (AMPK)mitochondrial uncouplernonalcoholic steatohepatitis (NASH)sorafenib

Identifiers

PMID32375062
PMCPMC9375823
OpenAlexW3022051450

What OpenQuestion holds

Textmetadata
LicenceTDM
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.