Evidence map›Paper›PMID 33173745›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

The Nuclear Orphan Receptor NR2F6 Promotes Hepatic Steatosis through Upregulation of Fatty Acid Transporter CD36.

Bing Zhou, Lijing Jia, Zhijian Zhang, Liping Xiang, Youwen Yuan, Peilin Zheng, Bin Liu, Xingxing Ren, Hua Bian, Liwei Xie and 4 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

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  6. Loss of NR2F6 Protects from Salmonella Typhimurium Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

14 authors at 5 institutions in 1 country.

Bing ZhouThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Lijing JiaDepartment of Endocrinology Shenzhen People's Hospital The Second Clinical Medical College, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology Shenzhen Guangdong 518020 P. R. China.
Zhijian ZhangDepartment of Endocrinology and Metabolism Shanghai General Hospital Shanghai Jiao Tong University School of Medicine Shanghai 201620 P. R. China.
Liping XiangThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Youwen YuanDepartment of Endocrinology and Metabolism Nanfang Hospital Southern Medical University Guangzhou Guangdong 510515 P. R. China.
Peilin ZhengDepartment of Endocrinology Shenzhen People's Hospital The Second Clinical Medical College, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology Shenzhen Guangdong 518020 P. R. China.
Bin LiuThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Xingxing RenThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Hua BianThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Liwei XieState Key Laboratory of Applied Microbiology Southern China Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application Guangdong Open Laboratory of Applied Microbiology Guangdong Institute of Microbiology Guangdong Academy of Sciences Guangzhou Guangdong 510070 P. R. China.
Yao LiDepartment of Laboratory Animal Science Shanghai Jiao Tong University School of Medicine Shanghai 200025 P. R. China.
Jieli LuDepartment of Endocrinology and Metabolism Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200025 P. R. China.
Huijie ZhangDepartment of Endocrinology and Metabolism Nanfang Hospital Southern Medical University Guangzhou Guangdong 510515 P. R. China.ORCID https://orcid.org/0000-0003-0640-0315
Yan LuThe Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education Department of Endocrinology and Metabolism Fudan Institute for Metabolic Diseases Zhongshan Hospital Fudan University Shanghai 230032 P. R. China.
Fudan University · CNShanghai Jiao Tong University · CNJinan University · CNNanfang Hospital · CNGuangdong Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear receptors (NRs) are a superfamily of transcription factors which sense hormonal signals or nutrients to regulate various biological events, including development, reproduction, and metabolism. Here, this study identifies nuclear receptor subfamily 2, group F, member 6 (NR2F6), as an important regulator of hepatic triglyceride (TG) homeostasis and causal factor in the development of non-alcoholic fatty liver disease (NAFLD). Adeno-associated virus (AAV)-mediated overexpression of NR2F6 in the liver promotes TG accumulation in lean mice, while hepatic-specific suppression of NR2F6 improves obesity-associated hepatosteatosis, insulin resistance, and methionine and choline-deficient (MCD) diet-induced non-alcoholic steatohepatitis (NASH). Mechanistically, the fatty acid translocase CD36 is identified as a transcriptional target of NR2F6 to mediate its steatotic role. NR2F6 is able to bind directly onto the CD36 promoter region in hepatocytes and increases the enrichment of nuclear receptor coactivator 1 (SRC-1) and histone acetylation at its promoter. Of pathophysiological significance, NR2F6 is significantly upregulated in the livers of obese mice and NAFLD patients. Moreover, treatment with metformin decreases NR2F6 expression in obese mice, resulting in suppression of CD36 and reduced hepatic TG contents. Therefore, these results provide evidence for an unpredicted role of NR2F6 that contributes to liver steatosis and suggest that NR2F6 antagonists may present a therapeutic strategy for reversing or treating NAFLD/NASH pathogenesis.

Indexed as

CD36non‐alcoholic fatty liver diseaseNR2F6nuclear receptorsobesity

Identifiers

PMID33173745
PMCPMC7610302
OpenAlexW3088815239

What OpenQuestion holds

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LicenceCC BY
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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.