Influence of coronary artery occlusion on apoptosis and activation of apoptosis proteins

Abstract

Cardiovascular diseases remain one of the main causes of morbidity and mortality worldwide. Two thirds of cardiovascular diseases are comprised by coronary artery disease (CAD, or ischemic heart disease, ischemia)/ myocardial infarction is the most severe complication of CAD. Now it is believed that massive cell loss due to apoptosis may contribute to the infarction size and may be responsible for remodeling occurring straight after infarction. Being highly regulated process apoptosis is controlled by large number of regulatory proteins. It is believed that Bcl-2 family proteins play essential role in apoptosis progression and subsequent caspase-3 activation, which is known to be in important execution step of cell death. In the given work using the myocardial infarction model we demonstrated that increased level of pro-apoptotic Bax protein and levels of active caspase-3 ware observed not only in infracted area itself but also in remote from the infraction areas. Therefore it was concluded that activation of Bax and decrease in anti apoptotic Bcl-2 protein can be important in triggering the caspase-3 cleavage and apoptosis induction in remote from infarction areas. Understanding of precise molecular mechanisms of cardiac remodeling can be helpful in designing novel therapeutical approaches in diseases treatment.