Evidence map›Paper›PMID 30820969›Full record

ArticleHepatology (Baltimore, Md.)2019

Dual Specificity Phosphatase 12 Regulates Hepatic Lipid Metabolism Through Inhibition of the Lipogenesis and Apoptosis Signal-Regulating Kinase 1 Pathways.

Zhen Huang, Lei-Ming Wu, Jie-Lei Zhang, Abdelkarim Sabri, Shou-Jun Wang, Gui-Jun Qin, Chang-Qing Guo, Hong-Tao Wen, Bin-Bin Du, Dian-Hong Zhang and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

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  14. CSAD Ameliorates Lipid Accumulation in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2022
    Article
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  16. Review
  17. Article
  18. Review
  19. Active p38α causes macrovesicular fatty liver in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 2 institutions in 2 countries.

Zhen HuangCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Lei-Ming WuCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Jie-Lei ZhangDepartment of Endocrinology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Abdelkarim SabriCardiovascular Research Center, Department of Physiology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA.
Shou-Jun WangDepartment of Endocrinology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Gui-Jun QinDepartment of Endocrinology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Chang-Qing GuoGastroenterology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Hong-Tao WenGastroenterology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Bin-Bin DuCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Dian-Hong ZhangCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Ling-Yao KongCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Xin-Yu TianCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Rui YaoCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Ya-Peng LiCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Cui LiangCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Peng-Cheng LiCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Zheng WangCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Jin-Yan GuoDepartment of Rheumatology and Immunology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Ling LiCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Jian-Zeng DongCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Yan-Zhou ZhangCardiovascular Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CNTemple University · US

Funding

Cooperative Project of Academy training Foundation of Zhengzhou University 2016-BSTDJJ-13National Natural Science Foundation of China 81770048
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease worldwide. Due to the growing economic burden of NAFLD on public health, it has become an emergent target for clinical intervention. DUSP12 is a member of the dual specificity phosphatase (DUSP) family, which plays important roles in brown adipocyte differentiation, microbial infection, and cardiac hypertrophy. However, the role of DUSP12 in NAFLD has yet to be clarified. Here, we reveal that DUSP12 protects against hepatic steatosis and inflammation in L02 cells after palmitic acid/oleic acid treatment. We demonstrate that hepatocyte specific DUSP12-deficient mice exhibit high-fat diet (HFD)-induced and high-fat high-cholesterol diet-induced hyperinsulinemia and liver steatosis and decreased insulin sensitivity. Consistently, DUSP12 overexpression in hepatocyte could reduce HFD-induced hepatic steatosis, insulin resistance, and inflammation. At the molecular level, steatosis in the absence of DUSP12 was characterized by elevated apoptosis signal-regulating kinase 1 (ASK1), which mediates the mitogen-activated protein kinase (MAPK) pathway and hepatic metabolism. DUSP12 physically binds to ASK1, promotes its dephosphorylation, and inhibits its action on ASK1-related proteins, JUN N-terminal kinase, and p38 MAPK in order to inhibit lipogenesis under high-fat conditions. Conclusion: DUSP12 acts as a positive regulator in hepatic steatosis and offers potential therapeutic opportunities for NAFLD.

Indexed as

Gene Expression RegulationAnalysis of VarianceAnimalsApoptosisCells, CulturedDiet, High-FatDisease Models, AnimalDown-RegulationDual-Specificity PhosphatasesHumansInsulin ResistanceLipid MetabolismLipogenesisMaleMAP Kinase Kinase Kinase 5MiceDual-Specificity PhosphatasesMap3k5 protein, mouseMAP Kinase Kinase Kinase 5

Identifiers

PMID30820969
PMCPMC6850665
OpenAlexW2920322608

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.