Evidence map›Paper›PMID 32657424›Full record

ArticleJournal of cellular physiology2021

GRP78 effectively protect hypoxia/reperfusion-induced myocardial apoptosis via promotion of the Nrf2/HO-1 signaling pathway.

Heyu Ji, Feng Xiao, Suobei Li, Ruan Wei, Fei Yu, Junmei Xu

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  16. Aconitine Induces TRPV2-Mediated CaEvidence-based complementary and alternative medicine : eCAM · 2021
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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

6 authors at 2 institutions in 1 country.

Heyu JiDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Feng XiaoDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Suobei LiDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ruan WeiDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Fei YuDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0002-9036-2464
Junmei XuDepartment of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Central South University · CNBinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction is a major cause of death worldwide. Despite our understanding of the pathophysiology of myocardial infarction and the therapeutic options for treatment have improved substantially, acute myocardial infarction remains a leading cause of morbidity and mortality. Recent findings revealed that GRP78 could protect myocardial cells against ischemia reperfusion injury-induced apoptosis, but the exact function and molecular mechanism remains unclear. In this study, we aimed to explore the effects of GRP78 on hypoxia/reperfusion (H/R)-induced cardiomyocyte injury. Intriguingly, we first observed that GRP78 overexpression significantly protected myocytes from H/R-induced apoptosis. On mechanism, our work revealed that GRP78 protected myocardial cells from hypoxia/reperfusion-induced apoptosis via the activation of the Nrf2/HO-1 signaling pathway. We observed the enhanced expression of Nrf2/HO-1 in GRP78 overexpressed H9c2 cell, while GRP78 deficiency dramatically antagonized the expression of Nrf2/HO-1. Furthermore, we found that blocked the Nrf2/HO-1 signaling by the HO-1 inhibitor zinc protoporphyrin IX (Znpp) significantly retrieved H9c2 cells apoptosis that inhibited by GRP78 overexpression. Taken together, our findings revealed a new mechanism by which GRP78 alleviated H/R-induced cardiomyocyte apoptosis in H9c2 cells via the promotion of the Nrf2/HO-1 signaling pathway.

Indexed as

AnimalsApoptosisCell HypoxiaCell LineCell SurvivalEndoplasmic Reticulum Chaperone BiPHeartHeat-Shock ProteinsHeme Oxygenase (Decyclizing)HumansMyocardial InfarctionMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressRatsReperfusion InjuryEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsHeme Oxygenase (Decyclizing)Hmox1 protein, ratHSPA5 protein, humanNfe2l2 protein, ratNF-E2-Related Factor 2apoptosisGRP78HO-1myocardial hypoxia/reperfusionNrf2

Identifiers

PMID32657424
PMCPMC7754434
OpenAlexW3043686868

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.