Evidence map›Paper›PMID 32155321›Full record

ReviewJournal of cellular and molecular medicine2020

Mitochondrial and mitochondrial-independent pathways of myocardial cell death during ischaemia and reperfusion injury.

Sean M Davidson, Adriana Adameová, Lucio Barile, Hector Alejandro Cabrera-Fuentes, Antigone Lazou, Pasquale Pagliaro, Kåre-Olav Stensløkken, David Garcia-Dorado, EU-CARDIOPROTECTION COST Action (CA16225)

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 3 pooled it
16.1field-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

127 citing papers in PubMed, 3 syntheses or guidelines pooled it, 196 citations in OpenAlex.

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  20. Mitophagy: a novel avenue for herbal medicines alleviating myocardial ischemia/reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025
    Review

67 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

9 authors at 7 institutions in 10 countries.

Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, London, UK.ORCID 0000-0001-5182-4980
Adriana AdameováFaculty of Pharmacy, Comenius University Bratislava, Bratislava, Slovakia.
Lucio BarileLaboratory for Cardiovascular Theranostics, Cardiocentro Ticino Foundation and Faculty of Biomedical Sciences, Università Svizzera Italiana, Lugano, Switzerland.
Hector Alejandro Cabrera-FuentesSingHealth Duke-NUS Cardiovascular Sciences Academic Clinical Programme and Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.ORCID 0000-0002-8502-7098
Antigone LazouSchool of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.ORCID 0000-0002-7889-9648
Pasquale PagliaroDepartment of Biological and Clinical Sciences, University of Turin, Torino, Italy.
Kåre-Olav StensløkkenSection of Physiology, Department of Molecular Medicine, Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway.
David Garcia-DoradoIIS-Fundación Jiménez Díaz University Hospital, Madrid, Spain.
EU-CARDIOPROTECTION COST Action (CA16225)
5T Torino (Italy) · ITAristotle University of Thessaloniki · GRCentre of Experimental Medicine of the Slovak Academy of Sciences · SKSingHealth · SGUniversitat Autònoma de Barcelona · ESUniversity College London · GBUniversity of Oslo · NO

Funding

British Heart Foundation PG/18/44/33790Department of Health BRC233/CM/SD/101320Swiss National Science Foundation IZCOZ0_182948/1
6 · The paper itself

Abstract

Acute myocardial infarction causes lethal injury to cardiomyocytes during both ischaemia and reperfusion (IR). It is important to define the precise mechanisms by which they die in order to develop strategies to protect the heart from IR injury. Necrosis is known to play a major role in myocardial IR injury. There is also evidence for significant myocardial death by other pathways such as apoptosis, although this has been challenged. Mitochondria play a central role in both of these pathways of cell death, as either a causal mechanism is the case of mitochondrial permeability transition leading to necrosis, or as part of the signalling pathway in mitochondrial cytochrome c release and apoptosis. Autophagy may impact this process by removing dysfunctional proteins or even entire mitochondria through a process called mitophagy. More recently, roles for other programmed mechanisms of cell death such as necroptosis and pyroptosis have been described, and inhibitors of these pathways have been shown to be cardioprotective. In this review, we discuss both mitochondrial and mitochondrial-independent pathways of the major modes of cell death, their role in IR injury and their potential to be targeted as part of a cardioprotective strategy. This article is part of a special Issue entitled 'Mitochondria as targets of acute cardioprotection' and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

Indexed as

ApoptosisAutophagyCell DeathHumansMitochondriaMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumNecrosisSignal Transductionapoptosisautophagycardiaccell deathischaemiamyocardial infarctionnecroptosisnecrosispyroptosisreperfusion

Identifiers

PMID32155321
PMCPMC7171390
OpenAlexW3011824135

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.