Evidence map›Paper›PMID 30804206›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Inhibition of soluble epoxide hydrolase attenuates a high-fat diet-mediated renal injury by activating PAX2 and AMPK.

Ying Luo, Ming-Yu Wu, Bing-Qing Deng, Jian Huang, Sung Hee Hwang, Meng-Yuan Li, Chun-Yu Zhou, Qian-Yun Zhang, Hai-Bo Yu, Da-Ke Zhao and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  7. Metabolomics reveals soluble epoxide hydrolase as a therapeutic target for high-sucrose diet-mediated gut barrier dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Soluble epoxide hydrolase-targeting PROTAC activates AMPK and inhibits endoplasmic reticulum stress.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Article
  10. Review
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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

15 authors at 3 institutions in 2 countries.

Ying LuoCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Ming-Yu WuCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Bing-Qing DengCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Jian HuangCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Sung Hee HwangDepartment of Entomology and Nematology, University of California, Davis, CA 95616.
Meng-Yuan LiCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Chun-Yu ZhouCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Qian-Yun ZhangCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Hai-Bo YuCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Da-Ke ZhaoCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Guodong ZhangDepartment of Food Science, University of Massachusetts, Amherst, MA 01003.ORCID 0000-0001-7780-5470
Ling QinCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Ai PengCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China.
Bruce D HammockDepartment of Entomology and Nematology, University of California, Davis, CA 95616; bdhammock@ucdavis.edu jyliu@tongji.edu.cn.ORCID 0000-0003-1408-8317
Jun-Yan LiuCenter for Nephrology and Metabolomics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 200072 Shanghai, People's Republic of China; bdhammock@ucdavis.edu jyliu@tongji.edu.cn.ORCID 0000-0002-3018-0335
Tongji University · CNUniversity of California, Davis · USUniversity of Massachusetts Amherst · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
OXYGENASE METABOLITES AND RENAL VASCULAR ACTIVITYR01HL059699 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI IMIG, JOHN D · 1999 to 2011
$3.0M
NHLBI NIH HHS R01 HL059699NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R01 ES002710
6 · The paper itself

Abstract

A high-fat diet (HFD) causes obesity-associated morbidities involved in macroautophagy and chaperone-mediated autophagy (CMA). AMPK, the mediator of macroautophage, has been reported to be inactivated in HFD-caused renal injury. However, PAX2, the mediator for CMA, has not been reported in HFD-caused renal injury. Here we report that HFD-caused renal injury involved the inactivation of Pax2 and Ampk, and the activation of soluble epoxide hydrolase (sEH), in a murine model. Specifically, mice fed on an HFD for 2, 4, and 8 wk showed time-dependent renal injury, the significant decrease in renal Pax2 and Ampk at both mRNA and protein levels, and a significant increase in renal sEH at mRNA, protein, and molecular levels. Also, administration of an sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea, significantly attenuated the HFD-caused renal injury, decreased renal sEH consistently at mRNA and protein levels, modified the renal levels of sEH-mediated epoxyeicosatrienoic acids (EETs) and dihydroxyeicosatrienoic acids (DHETs) as expected, and increased renal Pax2 and Ampk at mRNA and/or protein levels. Furthermore, palmitic acid (PA) treatment caused significant increase in

Indexed as

Diet, High-FatAdenylate KinaseAnimalsCytochrome P-450 Enzyme SystemDisease Models, AnimalEicosanoidsEnzyme InhibitorsEpoxide HydrolasesHypertrophyKidneyMesangial CellsMicePalmitic AcidPAX2 Transcription FactorPhenylurea CompoundsPiperidines1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)ureaAdenylate KinaseCytochrome P-450 Enzyme SystemEicosanoidsEnzyme InhibitorsEpoxide HydrolasesPalmitic AcidPAX2 Transcription FactorPhenylurea CompoundsPiperidinesautophagyeicosanoidslipidomicsmetabolomicsrenal hypertrophy

Identifiers

PMID30804206
PMCPMC6421466
OpenAlexW2915302248

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.