Sunday, September 8, 2019

Cellular Biology Article Discussion-Gene Sharing Yields an Enzyme with

Cellular Biology Discussion-Gene Sharing Yields an Enzyme with Two Binding Sites in One Subunit - Article Example It is well recognized that mitochondria have an important role to play in the development of reperfusion injury. Against this backdrop, the paper titled, â€Å"Mitochondrial Death Channels† by Webster, K.A., addresses the actual mechanism of mitochondrial action of promoting reperfusion injury. The important and individual roles played by two mitochondrial death channels, the mitochondrial permeability transition pore (mPTP) and the mitochondrial apoptosis channel (mAC) in the promotion of infarction are described. It explains in detail, how, during a heart attack, mPTP, under the regulation of calcium and oxidative stress, causes necrotic death while both mPTP and mAC channels are involved in apoptosis. 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 heart attack (Krijnen et al., 2002). Besides, apoptosis in cardiomyocytes is mediated by mitochondria through the two mitochondrial dea th channels namely, mPTP and mAC as shown in the current paper. Mitochondria are known to be important mediators of cardiac injury during ischemia and

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