Evidence map›Paper›PMID 25471136›Full record

ArticleScientific reports2014

Sevoflurane postconditioning protects rat hearts against ischemia-reperfusion injury via the activation of PI3K/AKT/mTOR signaling.

Jing Zhang, Chen Wang, Shuchun Yu, Zhenzhong Luo, Yong Chen, Qin Liu, Fuzhou Hua, Guohai Xu, Peng Yu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 88 citations in OpenAlex.

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  8. Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023
    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

9 authors at 3 institutions in 1 country.

Jing ZhangDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Chen WangDepartment of Anesthesiology, the Second Affiliate Hospital of Soochow University, Suzhou, 215000, China.
Shuchun YuDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Zhenzhong LuoDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Yong ChenDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Qin LiuDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Fuzhou HuaDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Guohai XuDepartment of Anesthesiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Peng YuDepartment of Cardiology, the Second Affiliate Hospital of Nanchang University, Nanchang, 330000, China.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway plays a key role in myocardial ischemia-reperfusion (I/R) injury. Mammalian target of rapamycin (mTOR), a downstream target of PI3K/AKT signaling, is necessary and sufficient to protect the heart from I/R injury. Inhaled anesthetic sevoflurane is widely used in cardiac surgeries because its induction and recovery are faster and smoother than other inhaled anesthetics. Sevoflurane proved capable of inducing postconditioning effects in the myocardium. However, the underlying molecular mechanisms for sevoflurane-induced postconditioning (SPC) were largely unclear. In the present study, we demonstrated that SPC protects myocardium from I/R injury with narrowed cardiac infarct focus, increased ATP content, and decreased cardiomyocyte apoptosis, which are mainly due to the activation of PI3K/AKT/mTOR signaling and the protection of mitochondrial energy metabolism. Application of dactolisib (BEZ235), a PI3K/mTOR dual inhibitor, abolishes the up-regulation of pho-AKT, pho-GSK, pho-mTOR, and pho-p70s6k induced by SPC, hence abrogating the anti-apoptotic effect of sevoflurane and reducing SPC-mediated protection of heart from I/R injury. As such, this study proved that PI3K/AKT/mTOR pathway plays an important role in SPC induced cardiac protection against I/R injury.

Indexed as

AnimalsApoptosisHeartIschemic PostconditioningMaleMethyl EthersMyocardial Reperfusion InjuryMyocardiumPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySevofluraneSignal TransductionTOR Serine-Threonine KinasesUp-RegulationMethyl EthersmTOR protein, ratPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSevofluraneTOR Serine-Threonine Kinases

Identifiers

PMID25471136
PMCPMC4255182
OpenAlexW1965174412

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.