Maintaining energy provision in the heart: the creatine kinase system in ischaemia-reperfusion injury and chronic heart failure.
Level 5 - mechanism / opinion, no new human data
Narrative review with mechanism-based reasoning and bench/imaging studies without systematic review methodology.
PubMed 38639724 · doi:10.1042/CS20230616
What was done
This narrative review summarizes preclinical models and human magnetic resonance spectroscopy studies investigating high-energy phosphate metabolism (ATP and phosphocreatine) and the creatine kinase (CK) phosphagen system during acute myocardial ischaemia-reperfusion injury and chronic heart failure.
What was found
No numerical data are reported in the abstract. Preclinical models demonstrate that augmenting the CK system reduces ischaemia-reperfusion injury and enhances functional recovery. In chronic heart failure, down-regulation of the CK system and adenine nucleotide depletion correlate with cardiac dysfunction; however, causal evidence from loss-of-function models remains equivocal. Proof-of-principle studies indicate that augmenting CK activity improves cardiac function and remodelling in failing hearts.
Why it matters
This review highlights the CK phosphagen system as a potential metabolic therapeutic target to improve cardiac function, while distinguishing well-established correlative observations from unproven causal mechanisms.
Limits
The paper is a narrative review without systematic search protocols, risk of bias assessments, or quantitative pooling. The abstract omits sample sizes and quantitative effect sizes. Furthermore, human evidence remains limited to observational spectroscopy, and loss-of-function preclinical models provide equivocal causal support.
Cited by
- supports Both myocardial contraction (systole) and myocardial relaxation (diastole) require active energy consumption.