Evidence map›Paper›PMID 22323534›Full record

ArticleCardiovascular research2012

Endogenous cardioprotection by ischaemic postconditioning and remote conditioning.

Weiwei Shi, Jakob Vinten-Johansen

Abstract read
In one paragraph

Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Ribosome biogenesis in disease: new players and therapeutic targets.Signal transduction and targeted therapy · 2023
    Review
  5. Review
  6. Article
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  11. Ischaemic conditioning and reperfusion injury.Nature reviews. Cardiology · 2016
    Review
  12. Article
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  15. Review
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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

2 authors.

Weiwei ShiDepartment of Surgery, Emory University School of Medicine, Atlanta, GA 30308-2225, USA.
Jakob Vinten-Johansen

Funding

NHLBI NIH HHS HL094373
6 · The paper itself

Abstract

Persistent myocardial ischaemia causes cell death if not rescued by early reperfusion. Millions of years in nature's laboratory have evolved protective responses that 'condition' the heart (and other tissues) to adapt to stressors, and these responses are applicable to the relatively new societal stress of myocardial ischaemia and reperfusion injury. Conditioning can be applied before (preconditioning), during (perconditioning), or after (postconditioning) the ischaemic stressor by imposing short periods of non-lethal ischaemia separated by brief periods of reperfusion. This conditioning protects multiple cell types and induces or rebalances a number of physiological and molecular pathways that ultimately attenuate necrosis and apoptosis. The seemingly disparate pathways may converge directly or indirectly on the mitochondria as a final effector, but other pathways not affecting mitochondria broaden the mechanisms of cardioprotection. The potential downsides of imposing even brief ischaemia directly on the heart somewhat tempered the enthusiasm for applying conditioning stimuli to the heart, but this hurdle was surmounted by applying ischaemia to remote organs and tissues in pre-, per-, and postconditioning. Although the clinical translation of remote per- and postconditioning has been rapid compared with classical preconditioning, there are numerous basic questions that require further investigation, and wider adoption awaits large-scale randomized clinical trials. Pharmacological mimetics may provide another important therapeutic approach by which to treat evolving myocardial infarction.

Indexed as

ApoptosisHumansIschemic PostconditioningIschemic PreconditioningMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumSignal TransductionMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore

Identifiers

PMID22323534
PMCPMC3331613

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.