Evidence map›Paper›PMID 32653860›Full record

ReviewEBioMedicine2020

Mitochondria in acute myocardial infarction and cardioprotection.

Chrishan J A Ramachandra, Sauri Hernandez-Resendiz, Gustavo E Crespo-Avilan, Ying-Hsi Lin, Derek J Hausenloy

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 1 pooled it
19.8field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 1 synthesis or guideline pooled it, 309 citations in OpenAlex.

  1. Pooled it
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  11. Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  19. Lactylation landscape of mitochondrial proteins in myocardial infarction.bioRxiv : the preprint server for biology · 2026
    Article
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137 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 4 countries.

Chrishan J A RamachandraNational Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore.
Sauri Hernandez-ResendizNational Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany.
Gustavo E Crespo-AvilanNational Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany.
Ying-Hsi LinNational Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore.
Derek J HausenloyNational Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Department of Biochemistry, Medical Faculty, Justus Liebig-University, Giessen, Germany; Yong Loo Lin School of Medicine, National University Singapore, Singapore; The Hatter Cardiovascular Institute, University College London, London, UK; Cardiovascular Research Center, College of Medical and Health Sciences, Asia University, Taiwan. Electronic address: derek.hausenloy@duke-nus.edu.sg.
National University of Singapore · SGAsia University · TW

Funding

British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1
6 · The paper itself

Abstract

Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such, new treatments are needed to protect the myocardium against the damaging effects of the acute ischaemia and reperfusion injury (IRI) that occurs in AMI, in order to reduce myocardial infarct (MI) size, preserve cardiac function, and improve patient outcomes. In this regard, cardiac mitochondria play a dual role as arbiters of cell survival and death following AMI. Therefore, preventing mitochondrial dysfunction induced by acute myocardial IRI is an important therapeutic strategy for cardioprotection. In this article, we review the role of mitochondria as key determinants of acute myocardial IRI, and we highlight their roles as therapeutic targets for reducing MI size and preventing HF following AMI. In addition, we discuss the challenges in translating mitoprotective strategies into the clinical setting for improving outcomes in AMI patients.

Indexed as

Cardiotonic AgentsHeart FailureHumansMitochondriaMolecular Targeted TherapyMyocardial InfarctionMyocardiumReperfusion InjuryCardiotonic AgentsAcute myocardial infarctionCalcium overloadCardioprotectionIschaemia-reperfusion injuryIschaemic heart diseaseMitochondriaOxidative stress

Identifiers

PMID32653860
PMCPMC7355051
OpenAlexW3041140855

What OpenQuestion holds

Textmetadata
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.