Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction.

Ischemia and reperfusion (IR) injury remains a major cause of morbidity and mortality and multiple molecular and cellular pathways have been implicated in this injury. We determined whether acute inhibition of excessive mitochondrial fission at the onset of reperfusion improves mitochondrial dysfunction and cardiac contractility postmyocardial infarction in rats.

Pubmed ID: 24103571 RIS Download