Evidence map›Paper›PMID 32490600›Full record

ReviewJournal of cellular and molecular medicine2020

Mitochondrial ion channels as targets for cardioprotection.

Derek J Hausenloy, Rainer Schulz, Henrique Girao, Brenda R Kwak, Diego De Stefani, Rosario Rizzuto, Paolo Bernardi, Fabio Di Lisa

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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
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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

8 authors at 5 institutions in 7 countries.

Derek J HausenloyCardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.
Rainer SchulzInstitute of Physiology, Justus-Liebig University Giessen, Giessen, Germany.
Henrique GiraoCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-5786-8447
Brenda R KwakDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Diego De StefaniDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Rosario RizzutoDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Paolo BernardiDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Fabio Di LisaDepartment of Biomedical Sciences, University of Padova, Padova, Italy.ORCID 0000-0003-0705-7539
University of Padua · ITAsia University · TWEscola Superior de Tecnologia da Saúde de Coimbra · PTJustus-Liebig-Universität Gießen · DEUniversity of Geneva · CH

Funding

British Heart Foundation CS/14/3/31002British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1Swiss National Science Foundation 310030E_176050Swiss National Science Foundation IZCOZ0_189878
6 · The paper itself

Abstract

Acute myocardial infarction (AMI) and the heart failure (HF) that often result remain the leading causes of death and disability worldwide. As such, new therapeutic targets need to be discovered to protect the myocardium against acute ischaemia/reperfusion (I/R) injury in order to reduce myocardial infarct (MI) size, preserve left ventricular function and prevent the onset of HF. Mitochondrial dysfunction during acute I/R injury is a critical determinant of cell death following AMI, and therefore, ion channels in the inner mitochondrial membrane, which are known to influence cell death and survival, provide potential therapeutic targets for cardioprotection. In this article, we review the role of mitochondrial ion channels, which are known to modulate susceptibility to acute myocardial I/R injury, and we explore their potential roles as therapeutic targets for reducing MI size and preventing HF following AMI.

Indexed as

AnimalsCalcium ChannelsCardiotonic AgentsHumansIon ChannelsMitochondria, HeartModels, BiologicalTranslational Research, BiomedicalCalcium ChannelsCardiotonic AgentsIon Channelsmitochondrial calcium uniporteracute ischaemia/reperfusion injurycardioprotectionMitochondriamitochondrial permeability transition pore

Identifiers

PMID32490600
PMCPMC7339171
OpenAlexW3031836786

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.