ABSTRACT
The international forum on cardiac remodeling has defined cardiac remodeling as “alterations in the genome expression, molecules, cells and interstitium that are manifested clinically as changes in the size, shape and function of the heart after cardiac injury”. Despite the multiple etiologies possible for cardiac injury, the remodeling process seems to be the final common pathway leading to heart failure. Myocyte death by necrosis is associated with the disruption of cell membrane and loss of cell contents. Causes of necrosis in failing heart may include ongoing ischemia, immunoinflammatory diseases, and chemical insults such as alcohol and doxorubicin toxicity. Apoptosis also leads to heart muscle cell loss. In acute myocardial infarction, there is necrosis of myocytes within the infarct zone. However, both immediately and later in the postinfarct course, there is evidence of apoptosis in the peri-infarct zone and in the myocardium remote from the infarct site. Autophagic machinery with the ubiquitin/protein degradation system is highly conserved through evolution.
