Apoptosis is an evolutionarily conserved mechanism for the selective removal of aging, damaged or otherwise unwanted cells. It's sometimes referred to as programmed cell death, and indeed, the process of apoptosis follows a controlled, predictable routine.
Apoptosis plays a fundamental role in many physiological processes such as tissue development, and the immune response. Thus, regulation of apoptosis is important for tissue homeostasis and its deregulation can lead to a variety of pathological conditions including carcinogenesis and chemo-resistance.
Apoptosis is mediated primarily through promoting or inhibiting the activation of caspases. Caspases are effectors of cell suicide and cleave multiple substrates, leading to biochemical and morphological changes including mitochondrial outer membrane permeabilization, cell membrane
remodeling and blebbing, cell shrinkage, nuclear condensation, and DNA fragmentation.In mammalian systems, the extrinsic death receptor pathway, the intrinsic mitochondrial pathway and endoplasmic reticulum pathway are the major signaling systems that result in the activation of the executioner/effector caspases and the consequent demise of the cell.
All pathways eventually lead to a common pathway or the execution phase of apoptosis. Understanding the apoptosis mechanisms is important and helpful to us in the understanding of the pathogenesis of conditions as a result of disordered apoptosis. Meanwhile, it may help in the development of drugs that target certain apoptotic genes or pathways.
Apoptosis is mediated primarily by promoting or inhibiting the activation of caspases. There are three common ways of apoptosis mediation: apoptosis mediated by mitochondria, apoptosis mediated by endoplasmic reticulum and apoptosis mediated by death receptor.
For the hot topic of crosstalk between autophagy and apoptosis, an intelligible guy has written a review about this topic.
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