Evidence map›Paper›PMID 28378042›Full record

ReviewCellular and molecular life sciences : CMLS2017

Mitochondrial permeability transition in cardiac ischemia-reperfusion: whether cyclophilin D is a viable target for cardioprotection?

Sabzali Javadov, Sehwan Jang, Rebecca Parodi-Rullán, Zaza Khuchua, Andrey V Kuznetsov

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.7field-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

50 citing papers in PubMed, 92 citations in OpenAlex.

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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 3 institutions in 3 countries.

Sabzali JavadovDepartment of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR 00936-5067, Puerto Rico. sabzali.javadov@upr.edu.
Sehwan JangDepartment of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR 00936-5067, Puerto Rico.
Rebecca Parodi-RullánDepartment of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR 00936-5067, Puerto Rico.
Zaza KhuchuaCincinnati Children's Research Foundation, University of Cincinnati, 240 Albert Sabin Way, Cincinnati, OH, 54229, USA.
Andrey V KuznetsovCardiac Surgery Research Laboratory, Department of Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria.
University of Puerto Rico System · PRInnsbruck Medical University · ATUniversity of Cincinnati · US

Funding

Mitochondrial Permeability Transition as a Target for Cardioprotection in Heart FSC1HL118669 · NHLBI · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI JAVADOV, SABZALI · 2012 to 2016
$1.3M
NHLBI NIH HHS SC1 HL118669
6 · The paper itself

Abstract

Growing number of studies provide strong evidence that the mitochondrial permeability transition pore (PTP), a non-selective channel in the inner mitochondrial membrane, is involved in the pathogenesis of cardiac ischemia-reperfusion and can be targeted to attenuate reperfusion-induced damage to the myocardium. The molecular identity of the PTP remains unknown and cyclophilin D is the only protein commonly accepted as a major regulator of the PTP opening. Therefore, cyclophilin D is an attractive target for pharmacological or genetic therapies to reduce ischemia-reperfusion injury in various animal models and humans. Most animal studies demonstrated cardioprotective effects of PTP inhibition; however, a recent large clinical trial conducted by international groups demonstrated that cyclosporine A, a cyclophilin D inhibitor, failed to protect the heart in patients with myocardial infarction. These studies, among others, raise the question of whether cyclophilin D, which plays an important physiological role in the regulation of cell metabolism and mitochondrial bioenergetics, is a viable target for cardioprotection. This review discusses previous studies to provide comprehensive information on the physiological role of cyclophilin D as well as PTP opening in the cell that can be taken into consideration for the development of new PTP inhibitors.

Indexed as

Drug DiscoveryAnimalsCalciumCardiotonic AgentsCyclophilinsEnergy MetabolismHeartHumansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMolecular Targeted TherapyMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumOxidative StressPeptidyl-Prolyl Isomerase FCalciumCardiotonic AgentsCyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FCardioprotectionCyclophilin DIschemia–reperfusion injuryMitochondrial permeability transition poresOxidative stress

Identifiers

PMID28378042
PMCPMC5977999
OpenAlexW2604677774

What OpenQuestion holds

Textmetadata
LicenceTDM
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.