Evidence map›Paper›PMID 31925563›Full record

ArticleBasic research in cardiology2020

Overexpression of mitochondrial creatine kinase preserves cardiac energetics without ameliorating murine chronic heart failure.

Fang Cao, Mahon L Maguire, Debra J McAndrew, Hannah A Lake, Stefan Neubauer, Sevasti Zervou, Jürgen E Schneider, Craig A Lygate

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Synergistic effect on cardiac energetics by targeting the creatine kinase system: in vivo application of high-resolutionJournal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2023
    Article
  6. Observational
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  20. The Pitfalls ofFrontiers in physiology · 2021
    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

8 authors at 2 institutions in 1 country.

Fang CaoDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Mahon L MaguireDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Debra J McAndrewDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Hannah A LakeDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Stefan NeubauerDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Sevasti ZervouDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Jürgen E SchneiderDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Craig A LygateDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK. clygate@well.ox.ac.uk.ORCID http://orcid.org/0000-0001-6079-0284
Centre for Human Genetics · GBUniversity of Leeds · GB

Funding

BHF Centre of Research Excellence, Oxford RE/13/1/30181British Heart Foundation FS/11/50/29038British Heart Foundation RG/13/8/30266British Heart Foundation RG/18/12/34040Wellcome TrustWellcome Trust 203141/Z/16/Z
6 · The paper itself

Abstract

Mitochondrial creatine kinase (Mt-CK) is a major determinant of cardiac energetic status and is down-regulated in chronic heart failure, which may contribute to disease progression. We hypothesised that cardiomyocyte-specific overexpression of Mt-CK would mitigate against these changes and thereby preserve cardiac function. Male Mt-CK overexpressing mice (OE) and WT littermates were subjected to transverse aortic constriction (TAC) or sham surgery and assessed by echocardiography at 0, 3 and 6 weeks alongside a final LV haemodynamic assessment. Regardless of genotype, TAC mice developed progressive LV hypertrophy, dilatation and contractile dysfunction commensurate with pressure overload-induced chronic heart failure. There was a trend for improved survival in OE-TAC mice (90% vs 73%, P = 0.08), however, OE-TAC mice exhibited greater LV dilatation compared to WT and no functional parameters were significantly different under baseline conditions or during dobutamine stress test. CK activity was 37% higher in OE-sham versus WT-sham hearts and reduced in both TAC groups, but was maintained above normal values in the OE-TAC hearts. A separate cohort of mice received in vivo cardiac

Indexed as

Energy MetabolismAnimalsChronic DiseaseCreatine Kinase, Mitochondrial FormDisease Models, AnimalHeart FailureHypertrophy, Left VentricularMaleMice, Inbred C57BLMice, TransgenicMitochondria, HeartMyocytes, CardiacSignal TransductionVentricular Dysfunction, LeftVentricular Function, LeftVentricular RemodelingCreatine Kinase, Mitochondrial FormCardiac energeticsCreatine kinaseHeart failureMetabolismTransgenic

Identifiers

PMID31925563
PMCPMC6954138
OpenAlexW2998734523

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Registered trials

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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.