Evidence map›Paper›PMID 24108764›Full record

ArticleJournal of the American Heart Association2013

Enoyl coenzyme a hydratase domain-containing 2, a potential novel regulator of myocardial ischemia injury.

Jianhai Du, Zhixin Li, Quan-Zhen Li, Tongju Guan, Qiuhui Yang, Hao Xu, Kirkwood A Pritchard, Amadou K S Camara, Yang Shi

Open access · goldAbstract readComparative Study
In one paragraph

Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.1field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Jianhai DuDepartment of Surgery, Medical College of Wisconsin, Milwaukee, WI.
Zhixin Li
Quan-Zhen Li
Tongju Guan
Qiuhui Yang
Hao Xu
Kirkwood A Pritchard
Amadou K S Camara
Yang Shi
Medical College of Wisconsin · USAurora Health Care · USThe University of Texas Southwestern Medical Center · US

Funding

Biophysics of HDL DysfunctionR01HL112270 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PRITCHARD, KIRKWOOD ARTHUR, SORCI-THOMAS, MARY G · 2012 to 2015
$2.5M
Hsp90, NOS3 and CardioprotectionR01HL080468 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI SHI, YANG · 2006 to 2009
$1.7M
Tissue Kallikrein In Immune Mediated NephritisR03AR055778 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI LI, QUAN-ZHEN · 2009 to 2011
$232k
NHLBI NIH HHS HL080468SNHLBI NIH HHS R01 HL080468NHLBI NIH HHS R01 HL112270NIAMS NIH HHS R03 AR055778
6 · The paper itself

Abstract

backgroundWe reported previously that Brown Norway (BN) rats are more resistant to myocardial ischemia/reperfusion (I/R) injury than are Dahl S (SS) rats. To identify the unique genes differentially expressed in the hearts of these rats, we used DNA microarray analysis and observed that enoyl coenzyme A hydratase-containing domain 2 (ECHDC2) is highly expressed (≈18-fold) in the SS hearts compared with the BN hearts. METHODS AND

resultsRT-PCR, Western blot, and immunohistochemistry analyses verified that ECHDC2 was highly expressed in SS hearts compared with the BN hearts. ECHDC2 gene locates at chromosome 5 of rat and is expressed in mitochondria of the heart, mainly in cardiomyocytes but not in cardiofibroblasts. Overexpression of ECHDC2 in cells increased susceptibility to I/R injury while knockdown of ECHDC2 enhanced resistance to I/R injury. Furthermore, we observed that left anterior descending coronary artery ligation-induced myocardial infarction was more severe in the SS hearts than in the BN hearts or SSBN5 hearts, which was built on SS rats but had the substitution of chromosome 5 from BN rats. We also demonstrated that ECHDC2 did not alter mitochondrial O2 consumption, metabolic intermediates and ATP production. By gas chromatography-mass spectrometry, we found that ECHDC2 overexpression increased the levels of the cellular branched chain amino acids leucine and valine.

conclusionECHDC2, a mitochondrial protein, may be involved in regulating cell death and myocardial injury. Its deficiency in BN rats contributes to their increased resistance to myocardial I/R compared with SS rats. ECHDC2 increases branched chain amino acid metabolism and appears to be a novel regulator linking cell metabolism with cardiovascular disease.

Indexed as

Disease Models, AnimalRats, Inbred BNRats, Inbred DahlAnimalsEnoyl-CoA HydrataseHydro-LyasesMaleMyocardial Reperfusion InjuryRatsEnoyl-CoA HydrataseHydro-Lyasesmethylglutaconyl-CoA hydratasebranched amino acid metabolismcell deathECHDC2ischemia/reperfusion injurymyocardial infarction

Identifiers

PMID24108764
PMCPMC3835224
OpenAlexW2157130211

What OpenQuestion holds

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LicenceCC BY-NC
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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.