Evidence map›Paper›PMID 24124583›Full record

ArticlePloS one2013

Hypercholesterolemic myocardium is vulnerable to ischemia-reperfusion injury and refractory to sevoflurane-induced protection.

Yong Xu, Lei-Lei Ma, Chen Zhou, Fei-Jiang Zhang, Fei-Juan Kong, Wen-Na Wang, Ling-Bo Qian, Can-Can Wang, Xian-Bao Liu, Min Yan and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  6. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
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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

11 authors at 3 institutions in 1 country.

Yong XuDepartment of Anesthesiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejaing, China.
Lei-Lei Ma
Chen Zhou
Fei-Jiang Zhang
Fei-Juan Kong
Wen-Na Wang
Ling-Bo Qian
Can-Can Wang
Xian-Bao Liu
Min Yan
Jian-An Wang
Second Affiliated Hospital of Zhejiang University · CNHangzhou Medical College · CNHangzhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have demonstrated that volatile anesthetic postconditioning confers myocardial protection against ischemia-reperfusion (IR) injury through activation of the reperfusion injury salvage kinase (RISK) pathway. As RISK has been shown to be impaired in hypercholesterolemia. Therefore, we investigate whether anesthetic-induced cardiac protection was maintained in hypercholesterolemic rats. In the present study, normocholesteolemic or hypercholesterolemic rat hearts were subjected to 30 min of ischemia and 2 h of reperfusion. Animals received 2.4% sevoflurane for 5 min or 3 cycles of 10-s ischemia/10-s reperfusion. The hemodynamic parameters, including left ventricular developed pressure, left ventricular end-diastolic pressure and heart rate, were continuously monitored. The infarct size, apoptosis, p-Akt, p-ERK1/2, p-GSK3β were determined. We found that both sevoflurane and ischemic postconditioning significantly improved heart pump function, reduced infarct size and increased the phosphorylation of Akt, ERK1/2 and their downstream target of GSK3β in the healthy rats. In the hypercholesterolemic rats, neither sevoflurane nor ischemic postconditioning improved left ventricular hemodynamics, reduced infarct size and increased the phosphorylated Akt, ERK1/2 and GSK3β. In contrast, GSK inhibitor SB216763 conferred cardioprotection against IR injury in healthy and hypercholesterolemic hearts. In conclusions, hyperchoesterolemia abrogated sevoflurane-induced cardioprotection against IR injury by alteration of upstream signaling of GSK3β and acute GSK inhibition may provide a novel therapeutic strategy to protect hypercholesterolemic hearts against IR injury.

Indexed as

Anesthetics, InhalationAnimalsApoptosisCardiotonic AgentsCoronary Artery DiseaseDietGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeart VentriclesHemodynamicsHypercholesterolemiaIschemic PostconditioningMaleMethyl EthersMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Anesthetics, InhalationCardiotonic AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratMethyl EthersMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSevoflurane

Identifiers

PMID24124583
PMCPMC3790738
OpenAlexW2016023882

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.