Evidence map›Paper›PMID 31967733›Full record

ReviewJournal of cellular and molecular medicine2020

Translational issues for mitoprotective agents as adjunct to reperfusion therapy in patients with ST-segment elevation myocardial infarction.

Hans Erik Bøtker, Hector Alejandro Cabrera-Fuentes, Marisol Ruiz-Meana, Gerd Heusch, Michel Ovize

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 61 citations in OpenAlex.

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  20. 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

5 authors at 5 institutions in 7 countries.

Hans Erik BøtkerDepartment of Cardiology, Aarhus University Hospital, Aarhus N, Denmark.ORCID 0000-0001-6358-8962
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.
Marisol Ruiz-MeanaVall d'Hebron Institut de Recerca, University Hospital Vall d'Hebron-Universitat Autònoma, Barcelona, Spain.
Gerd HeuschInstitute for Pathophysiology, West German Heart and Vascular Center, University of Essen. Medical School, Essen, Germany.
Michel OvizeCarMeN Laboratory, Hôpital Louis Pradel, Hospices Civils de Lyon, Université de Lyon and Explorations Fonctionnelles Cardiovasculaires, INSERM U1060, Lyon, France.
Aarhus University Hospital · DKCentro de Investigación en Red en Enfermedades Cardiovasculares · ESSingHealth · SGUniversité Claude Bernard Lyon 1 · FRWest German Heart and Vascular Center Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pre-clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI-9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co-medication into account may be of paramount importance during the design of pre-clinical and clinical studies testing mitoprotective drugs.

Indexed as

Myocardial ReperfusionTranslational Research, BiomedicalAnimalsClinical Trials as TopicHumansMitochondria, HeartProtective AgentsST Elevation Myocardial InfarctionProtective Agentscyclosporine Aischaemiamitochondriamyocardial infarctionreperfusion

Identifiers

PMID31967733
PMCPMC7077531
OpenAlexW3001901076

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.