Key result
Cardiac-specific overexpression of myofibrillar creatine kinase significantly improved post-ischemic functional recovery to 64.9% of preischemic levels compared to 13.7% in control hearts.
Why the study?
Does cardiac-specific CKM overexpression improve ATP kinetics and contractile function in postischemic myocardium in mice?
Population
Isolated, retrograde-perfused hearts from double-transgenic mice overexpressing the myofibrillar isoform of…
Comparison
Cardiac-specific overexpression of the… vs Age-matched littermates expressing only tTA fed…
Design
Preclinical
Follow-up
25 min ischemia followed by 40 min reperfusion
Authors
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May support CKM-targeted cardioprotection in ischemia; leaves open translation from murine models to clinical use.
Does cardiac-specific CKM overexpression improve ATP kinetics and contractile function in postischemic myocardium in mice?
Absolute Event Rate: 64.9% vs 13.7%
p-value: p=<0.01
Augmenting cardiac CKM expression attenuates ischemic acidosis, reduces injury, and improves ATP synthesis and contractile function recovery in postischemic myocardium.
Akki et al. (2012) studied Myocardial ischemia-reperfusion injury (n=10). Cardiac-specific overexpression of myofibrillar creatine kinase (CKM) vs. Control mice expressing only tTA was evaluated on Post-ischemic functional recovery (% preischemic rate pressure product) (p=<0.01). Cardiac-specific overexpression of myofibrillar creatine kinase significantly improved post-ischemic functional recovery to 64.9% of preischemic levels compared to 13.7% in control hearts.