Evidence map›Paper›PMID 27644317›Full record

ArticleScientific reports2016

HSPA12B Attenuated Acute Myocardial Ischemia/reperfusion Injury via Maintaining Endothelial Integrity in a PI3K/Akt/mTOR-dependent Mechanism.

Qiuyue Kong, Leyang Dai, Yana Wang, Xiaojin Zhang, Chuanfu Li, Surong Jiang, Yuehua Li, Zhengnian Ding, Li Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Research progress of quercetin in cardiovascular disease.Frontiers in cardiovascular medicine · 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 2 institutions in 2 countries.

Qiuyue KongDepartment of Anesthesiology, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Leyang DaiDepartment of Anesthesiology, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Yana WangDepartment of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Xiaojin ZhangDepartment of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Chuanfu LiDepartments of Surgery, East Tennessee State University, Johnson City, TN37614, USA.
Surong JiangDepartment of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Yuehua LiDepartment of Pathophysiology, Nanjing Medical University, Nanjing 210029, China.
Zhengnian DingDepartment of Anesthesiology, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Li LiuDepartment of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
Nanjing Medical University · CNEast Tennessee State University · US

Funding

Innate Immunity and Cardiovascular Function in SepsisR01GM083016 · NIGMS · EAST TENNESSEE STATE UNIVERSITY · PI LI, CHUANFU, WILLIAMS, DAVID L. · 2009 to 2021
$3.8M
NIGMS NIH HHS R01 GM083016
6 · The paper itself

Abstract

Endothelial damage is a critical mediator of myocardial ischemia/reperfusion (I/R) injury. HSPA12B is an endothelial-cell-specifically expressed heat shock protein. However, the roles of HSPA12B in acute myocardial I/R injury is unknown. Here we reported that myocardial I/R upregulated HSPA12B expression in ventricular tissues, and endothelial overexpression of HSPA12B in transgenic mice (Tg) limited infarct size, attenuated cardiac dysfunction and improved cardiomyocyte survival compared with their wild type littermates. These improvements were accompanied with the diminished myocardial no-reflow phenomenon, decreased microvascular leakage, and better maintained endothelial tight junctions. The I/R-evoked neutrophil infiltration was also suppressed in Tg hearts compared with its wild type (WT) littermates. Moreover, Tg hearts exhibited the enhanced activation of PI3K/Akt//mTOR signaling following I/R challenge. However, pharmacological inhibition of PI3K abolished the HSPA12B-induced cardioprotection against myocardial I/R injury. The data demonstrate for the first time that the endothelial HSPA12B protected hearts against myocardial I/R injury. This cardioprotective action of HSPA12B was mediated, at least in part, by improving endothelial integrity in a PI3K/Akt/mTOR-dependent mechanism. Our study suggests that targeting endothelial HSPA12B could be an alternative approach for the management of patients with myocardial I/R injury.

Indexed as

AnimalsApoptosisCell SurvivalDisease Models, AnimalEndotheliumGene Expression RegulationHSP70 Heat-Shock ProteinsHumansMaleMiceMice, TransgenicMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNeutrophil InfiltrationPhosphatidylinositol 3-KinasesHSP70 Heat-Shock ProteinsHSPA12B protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Cell Adhesion Molecule-1

Identifiers

PMID27644317
PMCPMC5028890
OpenAlexW2522810074

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.