Apoptotic cardiac cell demise has been demonstrated in myocardial tissues obtained from patients with congestive heart failure, acute myocardial infraction, arrhythmogenic right ventricular dysplasia, myocarditis, chemotherapy induced cardiomyopathies, diabetic cardiomyopathy, and so forth. Further, loss of functional capacity of the myocytes from apoptotic injury accounts for the major cause of morbidity and mortality in the above-mentioned heart diseases. Thus prevention of cardiomyocyte cell death (preserving functional myocardium) could have profound clinical implications in the treatment of acute myocardial infraction, heart failure, and so forth.

However, the development of specific inhibitors of cardiomyocyte apoptosis is currently restricted by our limited understanding of the signaling process involved in this process. In addition, the individual factors, that trigger and mediate the apoptotic cell death in the myocardium, are also murky. In light of these challenges, we invite investigators to contribute their critical review articles and original contributions that will stimulate our continuing efforts to understand the molecular and cellular pathophysiological mechanisms and impairments that culminate in the cardiomyocyte demise.

Potential topics include, but are not limited to:

• Oxidative stress induced redox-signaling and apoptosis in the myocardium
• Molecular triggers, mediators, and regulators of apoptotic cell death in the myocardium
• Role of mitochondria derived reactive oxygen free radicals in the myocardial cell death
• Advances in the development and utility of novel in vitro and preclinical experimental models to investigate and understand the pathophysiology of apoptotic myocardial cell death
• Biomarkers for cardiomyocyte cell death and prototype developments (small molecule inhibitors) to mitigate cardiomyocyte apoptosis
• Other modes of treatment approaches such as cell based therapies (stem cells) and use of plant derived chemicals (phytochemicals) to repair the injured myocardium and prevent the myocardial cell death