Evidence map›Paper›PMID 25393318›Full record

ReviewBritish journal of pharmacology2015

Role of the MPTP in conditioning the heart - translatability and mechanism.

S-B Ong, R K Dongworth, H A Cabrera-Fuentes, D J Hausenloy

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Pharmaceuticals (Basel, Switzerland) · 2025
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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

4 authors at 2 institutions in 3 countries.

S-B OngThe Hatter Cardiovascular Institute, University College London, London, UK.
R K Dongworth
H A Cabrera-Fuentes
D J Hausenloy
University College London · GBJustus-Liebig-Universität Gießen · DE

Funding

Biotechnology and Biological Sciences Research CouncilBritish Heart Foundation FS/10/39/28270British Heart Foundation FS/10/72/28568British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1
6 · The paper itself

Abstract

Mitochondria have long been known to be the gatekeepers of cell fate. This is particularly so in the response to acute ischaemia-reperfusion injury (IRI). Following an acute episode of sustained myocardial ischaemia, the opening of the mitochondrial permeability transition pore (MPTP) in the first few minutes of reperfusion, mediates cell death. Preventing MPTP opening at the onset of reperfusion using either pharmacological inhibitors [such as cyclosporin A (CsA) ] or genetic ablation has been reported to reduce myocardial infarct (MI) size in animal models of acute IRI. Interestingly, the endogenous cardioprotective intervention of ischaemic conditioning, in which the heart is protected against MI by applying cycles of brief ischaemia and reperfusion to either the heart itself or a remote organ or tissue, appears to be mediated through the inhibition of MPTP opening at reperfusion. Small proof-of-concept clinical studies have demonstrated the translatability of this therapeutic approach to target MPTP opening using CsA in clinical settings of acute myocardial IRI. However, given that CsA is a not a specific MPTP inhibitor, more novel and specific inhibitors of the MPTP need to be discovered - the molecular identification of the MPTP should facilitate this. In this paper, we review the role of the MPTP as a target for cardioprotection, the potential mechanisms underlying MPTP inhibition in the setting of ischaemic conditioning, and the translatability of MPTP inhibition as a therapeutic approach in the clinical setting.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsHumansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryMyocardiumMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore

Identifiers

PMID25393318
PMCPMC4386982
OpenAlexW2112259462

What OpenQuestion holds

Textmetadata
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.