We have published proof of concept studies that mitochondrial DNA (mtDNA) escapes from necrotic tissue after myocardial infarction in STEMI patients, that mtDNA is taken up, are detrimental in an in vitro assay of adult mice cardiomyocyte and activate NFkB. We have also showed that of mtDNA oxidative base lesions may not be important for maintenance of cardiac function during IR injury in vivo.
We have showed inadvertent phosphorylation of protective protein kinases in the isolated perfused mouse and rat heart, which may influence on studies on cardioprotection. In a follow up we showed that parts of the endocard were not perfused during reperfusion. This implies that parts of the myocardial tissue are not exposed to reperfusion injury, but rather ischemic damage. This will again affect the molecular state of the heart, and may lead to wrong conclusions during such experiments.