Evidence map›Paper›PMID 22223859›Full record

ArticleJournal of lipid research2012

Epoxyeicosatrienoic acids protect rat hearts against tumor necrosis factor-α-induced injury.

Gang Zhao, Jianing Wang, Xizhen Xu, Yanyan Jing, Ling Tu, Xuguang Li, Chen Chen, Katherine Cianflone, Peihua Wang, Ryan T Dackor and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 61 citations in OpenAlex.

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  15. Orally Active Epoxyeicosatrienoic Acid Analogs.Journal of cardiovascular pharmacology · 2017
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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

12 authors at 5 institutions in 3 countries.

Gang ZhaoDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Jianing WangDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Xizhen XuDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Yanyan JingDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Ling TuDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China. Electronic address: proftu@tom.com.
Xuguang LiDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Chen ChenDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Katherine CianfloneCentre de Recherche Institut Universitaire de Cardiologie et Pneumologie de Quebec Universite Laval, Québec City, Québec G1V 4G5, Canada.
Peihua WangDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Ryan T DackorDivision of Intramural Research National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
Darryl C ZeldinDivision of Intramural Research National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
Dao Wen WangDepartment of Internal Medicine and Gene Therapy Center Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China; Centre de Recherche Institut Universitaire de Cardiologie et Pneumologie de Quebec Universite Laval, Québec City, Québec G1V 4G5, Canada. Electronic address: dwwang@tjh.tjmu.edu.cn.
Huazhong University of Science and Technology · CNTongji Hospital · CNInstitut Universitaire de Cardiologie et de Pneumologie de Québec · CANational Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Characterization And Functional Significance Of P450 Arachidonate EpoxygenasesZIAES025034 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 2009 to 2025
$18.6M
Intramural NIH HHS
6 · The paper itself

Abstract

Epoxyeicosatrienoic acids (EET), the primary arachidonic acid metabolites of cytochrome P450 2J (CYP2J) epoxygenases, possess potent vasodilatory, anti-inflammatory, antiapoptotic, and mitogenic effects. To date, little is known about the role of CYP2J2 and EETs in tumor necrosis factor (TNF)-α-induced cardiac injury. We utilized cell culture and in vivo models to examine the effects of exogenously applied EETs or CYP2J2 overexpression on TNF-α-induced cardiac apoptosis and cardiac dysfunction. In neonatal rat cardiomyocytes, TNF-α-induced apoptosis was markedly attenuated by EETs or CYP2J2 overexpression, leading to significantly improved cell survival. Further studies showed that TNF-α decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL, decreased IκBα and PPARγ, and also inhibited PI3K-dependent Akt and EGFR signaling. Both EETs and CYP2J2 overexpression reversed the effects of TNF-α on these pathways. Furthermore, overexpression of CYP2J2 in rats prevented the decline in cardiac function that is normally observed in TNF-α-challenged animals. These results demonstrate that EETs or CYP2J2 overexpression can prevent TNF-α-induced cardiac cell injury and cardiac dysfunction by inhibiting apoptosis, reducing inflammation, and enhancing PPARγ expression. Targeting the CYP2J2 epoxygenase pathway may represent a novel approach to mitigate cardiac injury in diseases such as heart failure, where increased TNF-α levels are known to occur.

Indexed as

8,11,14-Eicosatrienoic AcidAnimalsAnimals, Genetically ModifiedAnimals, NewbornApoptosisCell LineCells, CulturedCytochrome P-450 Enzyme SystemEicosanoidsFlow CytometryHeartHemodynamicsMalePeroxisome Proliferator-Activated ReceptorsRatsRats, Sprague-Dawley14,15-dihydroxyeicosatrienoic acid8,11,14-Eicosatrienoic AcidCytochrome P-450 Enzyme SystemEicosanoidsPeroxisome Proliferator-Activated ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID22223859
PMCPMC3276469
OpenAlexW2102011208

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.