Evidence map›Paper›PMID 21955136›Full record

ReviewBritish journal of pharmacology2012

Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent.

Derek J Hausenloy, E A Boston-Griffiths, D M Yellon

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

Review in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
6.5field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
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  12. Review
  13. Cardiovascular effects of immunosuppression agents.Frontiers in cardiovascular medicine · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. COVID-19 therapy: What weapons do we bring into battle?Bioorganic & medicinal chemistry · 2020
    Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Derek J HausenloyThe Hatter Cardiovascular Institute, University College London Hospital & Medical School, London, UK. d.hausenloy@ucl.ac.uk
E A Boston-Griffiths
D M Yellon
University College Hospital · GBUniversity College Hospital at Westmoreland Street · GBUniversity College London · GB

Funding

British Heart Foundation FS/10/039/28270British Heart Foundation RG/03/007British Heart Foundation RG/08/015/26411Department of Health
6 · The paper itself

Abstract

Ischaemic heart disease (IHD) is the leading cause of death and disability worldwide. The pathophysiological effects of IHD on the heart most often result from the detrimental effects of acute ischaemia-reperfusion injury (IRI) on the myocardium. Therefore, novel therapeutic targets for protecting the myocardium against acute IRI are required to reduce injury to the heart, preserve cardiac function and improve clinical outcomes in patients with IHD. In this regard, the mitochondrial permeability transition pore (mPTP) has emerged as a critical target for cardioprotection which is readily amenable to intervention at the time of myocardial reperfusion. The formation and opening of the mPTP at the onset of myocardial reperfusion is a major determinant of mitochondrial dysfunction and cardiomyocyte death in the setting of acute IRI. The seminal discovery in the late 1980s that mPTP opening could be pharmacologically inhibited by the immunosuppressive agent, cyclosporin A (CsA), has been fundamental in the elucidation of the critical role of the mPTP as a mediator of acute IRI and, therefore, a viable target for cardioprotection. Its initial role as an investigative tool was used to identify mitochondrial cyclophilin D to be a regulatory component of the mPTP. The mPTP as a viable target for cardioprotection has recently been translated into the clinical setting with CsA reducing myocardial infarct size in patients. In this article, we review the intriguing role of CsA as a tool for investigating the mPTP as a target for cardioprotection and its potential role as a therapeutic agent for patients with IHD.

Indexed as

AnimalsCardiotonic AgentsCyclosporineHumansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial IschemiaMyocardiumCardiotonic AgentsCyclosporineMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore

Identifiers

PMID21955136
PMCPMC3372712
OpenAlexW1525029829

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.