1. Introduction
2. Programmed cell death occurs through Apoptosis
3. Discovery and etymology
4. Cell termination
5. Homeostasis
6. Development
7. Lymphocyte interactions
8. Process
9. Direct signal transduction
10. Execution
11. Three classes of Proteins function in the apoptotic Pathway
12. HIV progression
13. Viral infection
14. Pro-Apoptotic regulators promote caspase activation
15. Some trophic factors prevent apoptosis by inducing
16. Inactivation of a pro-apoptotic regulator
17. Mitochondrial regulation
18. Cell death and its regulation.Removal of dead cells
19. Defective apoptotic pathways
20. Bibliography

Apoptosis

Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death, in more specific terms, a series of biochemical events that lead to a variety of morphological changes, including blebbing, changes to the cell membrane such as loss of membrane asymmetry and attachment, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation (1-4). Processes of disposal of cellular debris whose results do not damage the organism differentiate apoptosis from necrosis.

In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis, in general, confers advantages during an organism’s life cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. Between 50 billion and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day. In a year, this amounts to the proliferation and subsequent destruction of a mass of cells equal to an individual’s body weight.

Research on apoptosis has increased substantially since the early 1990s. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases. Excessive apoptosis causes hypotrophy, such as in ischemic damage, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer.

Programmed Cell Death Occurs through Apoptosis

The demise of cells by programmed cell death is marked by a well-defined sequence of morphological changes, collectively referred to as apoptosis, a Greek word that means “dropping off” or “falling off” as in leaves from a tree. Dying cells shrink and condense and then fragment, releasing small membrane-bound apoptotic bodies, which generally are phagocytosed by other cells. Importantly, the intracellular constituents are not released into the extracellular milieu where they might have deleterious effects on neighboring cells. The highly stereotyped changes accompanying apoptosis suggested to early workers that this type of cell death was under the control of a strict cellular program.

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