Mitochondrial Death Channels by K.Webster - Article Example

Apoptosis or programmed cell death is an intrinsic cellular process, just as mitosis is. Cell suicides are resorted to in the course of development, for example, resorption of the tadpole tail during metamorphosis into a frog, or to destroy cells that represent a threat to the integrity of the organism, or when signals needed for continued survival are lacking. Apoptosis is different from necrosis in that it affects individual cells whereas necrosis affects groups of contiguous cells. Cardiovascular diseases which are the leading cause of death in all developed countries are characterized by the loss of cardiomyocytes due to cell death.

Earlier, cell death in myocardial infarction was believed to be caused solely by necrosis. However, recent studies have shown the involvement of apoptosis, too, in the process of myocardial tissue damage subsequent to a heart attack (Krijnen et al., 2002). Besides, apoptosis in cardiomyocytes is mediated by mitochondria through the two mitochondrial death channels namely, mPTP and mAC as shown in the current paper. Mitochondria are known to be important mediators of cardiac injury during ischemia and reperfusion (Chen et al., 2006). The electron transport chain undergoes a blockade due to lack of oxygen during myocardial ischemia (Chen et al.

, 2006; Webster, 2009) while, during reperfusion, a spurt in reactive oxygen species occurs because of an overwhelmed antioxidant system leading to oxidative stress and initiation of reperfusion injury. Mitochondrial calcium overload is also a central feature of cardiomyocyte death following reperfusion. The free radicals of oxygen together with calcium ions target the first mitochondrial death channel, mPTP causing it to open, triggering cell death. Conclusion In conclusion, the fact that the opening of the mitochondrial death channels is associated with both the processes believed to cause reperfusion injury, that is, classical apoptosis and programmed necrosis, has therapeutic implications.

Therapies designed to minimize the extent of either could hold promise for acute coronary syndromes. Indeed, some pharmacological compounds are already known (e.g., cyclosporine A, currently used as an immunosuppressant and sildenafil citrate, an approved drug for erectile dysfunction) that have the potential to curtail the opening of the mitochondrial death channels, and thereby reduce tissue damage due to heart attack. Mitochondrial damage is the cause of several other diseases as well. Yet very few therapies that target mitochondria have been developed because of problems associated with delivering the drugs to mitochondria in vivo (Smith et al., 2003).