Evidence map›Paper›PMID 30242115›Full record

ReviewBiochemical Society transactions2018

The creatine kinase system as a therapeutic target for myocardial ischaemia-reperfusion injury.

Fang Cao, Sevasti Zervou, Craig A Lygate

Open access · hybridAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Molecular medicine reports · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Energetic Interactions Between Subcellular Organelles in Striated Muscles.Frontiers in cell and developmental biology · 2020
    Review
  14. Review
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 2 institutions in 1 country.

Fang CaoDivision of Cardiovascular Medicine, Radcliffe Department of Medicine and the BHF Centre of Research Excellence, University of Oxford, Oxford, U.K.
Sevasti ZervouDivision of Cardiovascular Medicine, Radcliffe Department of Medicine and the BHF Centre of Research Excellence, University of Oxford, Oxford, U.K.
Craig A LygateDivision of Cardiovascular Medicine, Radcliffe Department of Medicine and the BHF Centre of Research Excellence, University of Oxford, Oxford, U.K. craig.lygate@cardiov.ox.ac.uk.ORCID 0000-0001-6079-0284
John Radcliffe Hospital · GBCentre for Human Genetics · GB

Funding

British Heart Foundation RG/13/8/30266Wellcome Trust 203141/Z/16/Z
6 · The paper itself

Abstract

Restoring blood flow following an acute myocardial infarction saves lives, but results in tissue damage due to ischaemia-reperfusion injury (I/R). Ameliorating this damage is a major research goal to improve recovery and reduce subsequent morbidity due to heart failure. Both the ischaemic and reperfusion phases represent crises of cellular energy provision in which the mitochondria play a central role. This mini-review will explore the rationale and therapeutic potential of augmenting the creatine kinase (CK) energy shuttle, which constitutes the primary short-term energy buffer and transport system in the cardiomyocyte. Proof-of-principle data from several transgenic mouse models have demonstrated robust cardioprotection by either raising myocardial creatine levels or by overexpressing specific CK isoforms. The effect on cardiac function, high-energy phosphates and myocardial injury will be discussed and possible directions for future research highlighted. We conclude that the CK system represents a viable target for therapeutic intervention in I/R injury; however, much needed translational studies will require the development of new pharmacological tools.

Indexed as

Myocardial Reperfusion InjuryAnimalsCreatine KinaseHeart FailureHumansMiceMice, TransgenicMitochondria, LiverMyocardial InfarctionMyocardiumMyocytes, CardiacPhosphatesReperfusion InjuryTranslational Research, BiomedicalCreatine KinasePhosphatesbioenergeticscardioprotectioncreatine kinaseischaemia–reperfusion injury

Identifiers

PMID30242115
PMCPMC6195634
OpenAlexW2889569875

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.