Key result
Creatine transporter overexpression significantly improved functional recovery following ischaemia-reperfusion injury in hypertrophied mouse hearts compared to wild-type controls (76% vs 59% of baseline, P=0.02).
Why the study?
Does elevated intracellular creatine protect against ischemia-reperfusion injury in the presence of comorbidities (LVH, aging) and during hypothermic cardioplegia in mouse models?
Population
Mice over-expressing the creatine transporter and wild-type littermates, including models of compensated…
Comparison
Genetic over-expression of the creatine… vs Wild-type littermates with normal intracellular…
Design
Preclinical, All experiments and analysis were performed by a single…
Follow-up
30 minutes reperfusion
Authors
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Hypothesis-generating for creatine transporter modulation in hypertrophy; leaves open translation to human ischaemia-reperfusion injury.
Does elevated intracellular creatine protect against ischemia-reperfusion injury in the presence of comorbidities (LVH, aging) and during hypothermic cardioplegia in mouse models?
Absolute Event Rate: 76% vs 59%
p-value: p=0.02
Elevating intracellular creatine preserves its cardioprotective effects against ischemia-reperfusion injury even in the presence of aging, left ventricular hypertrophy, and hypothermic cardioplegia in mouse models.
Whittington et al. (2016) studied Ischaemia-reperfusion injury (n=85). Creatine transporter overexpression vs. Wild-type littermates was evaluated on Functional recovery (Rate pressure product) during reperfusion in hearts with left ventricular hypertrophy (p=0.02). Creatine transporter overexpression significantly improved functional recovery following ischaemia-reperfusion injury in hypertrophied mouse hearts compared to wild-type controls (76% vs 59% of baseline, P=0.02).