Over-expression of mitochondrial creatine kinase in the murine heart improves functional recovery and protects against injury following ischaemia –reperfusion

ConclusionsModest elevation of MtCK activity in the heart does not adversely affect cellular metabolism, mitochondrial orin vivo cardiac function, but modifies mPTP opening to protect against I/R injury and improve functional recovery. Our findings support MtCK as a prime therapeutic target in myocardial ischaemia.
Source: Cardiovascular Research - Category: Cardiology Source Type: research