Evidence map›Paper›PMID 37955687›Full record

ArticleBasic research in cardiology2023

Targeting mitochondrial shape: at the heart of cardioprotection.

Sauri Hernandez-Resendiz, Aishwarya Prakash, Sze Jie Loo, Martina Semenzato, Kroekkiat Chinda, Gustavo E Crespo-Avilan, Linh Chi Dam, Shengjie Lu, Luca Scorrano, Derek J Hausenloy

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
7.8field-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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  7. Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

10 authors at 5 institutions in 4 countries.

Sauri Hernandez-ResendizDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Aishwarya PrakashDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Sze Jie LooDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Martina SemenzatoVeneto Institute of Molecular Medicine, Padova, Italy.
Kroekkiat ChindaDepartment of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.
Gustavo E Crespo-AvilanDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Linh Chi DamDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Shengjie LuDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore.
Luca ScorranoVeneto Institute of Molecular Medicine, Padova, Italy.
Derek J HausenloyDuke-NUS Medical School, Cardiovascular and Metabolic Disorders Programme, Singapore, Singapore. derek.hausenloy@duke-nus.edu.sg.ORCID http://orcid.org/0000-0003-0729-4956
Duke-NUS Medical School · SGNaresuan University · THNational University of Singapore · SGUniversity of Padua · ITVeneto Institute of Molecular Medicine · IT

Funding

Institutional Clinical and Translational Science AwardUL1TR000003 · NCATS · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2012 to 2015
$38.9M
6 · The paper itself

Abstract

There remains an unmet need to identify novel therapeutic strategies capable of protecting the myocardium against the detrimental effects of acute ischemia-reperfusion injury (IRI), to reduce myocardial infarct (MI) size and prevent the onset of heart failure (HF) following acute myocardial infarction (AMI). In this regard, perturbations in mitochondrial morphology with an imbalance in mitochondrial fusion and fission can disrupt mitochondrial metabolism, calcium homeostasis, and reactive oxygen species production, factors which are all known to be critical determinants of cardiomyocyte death following acute myocardial IRI. As such, therapeutic approaches directed at preserving the morphology and functionality of mitochondria may provide an important strategy for cardioprotection. In this article, we provide an overview of the alterations in mitochondrial morphology which occur in response to acute myocardial IRI, and highlight the emerging therapeutic strategies for targeting mitochondrial shape to preserve mitochondrial function which have the future therapeutic potential to improve health outcomes in patients presenting with AMI.

Indexed as

Heart FailureMyocardial InfarctionHumansMitochondriaMyocardiumMyocytes, CardiacAcute myocardial infarctionAcute myocardial ischemia–reperfusion injuryCardioprotectionCardiovascular diseasesHeart failureMitochondrial morphology

Identifiers

PMID37955687
PMCPMC10643419
OpenAlexW4388630445

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.