Apoptosis
Apoptosis is a form of programmed cell death that occurs in multicellular organisms and in some eukaryotic, single-celled microorganisms such as yeast.[1] Biochemical events lead to characteristic cell changes (morphology) and death.[2] These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation, and mRNA decay. The average adult human loses between 50 and 70 billion cells each day due to apoptosis. (Note that the average human adult has more than 13 trillion cells (Template:val),Template:sfn of which at most only 70 billion (Template:val) die per day. That is, about 5 out of every 1,000 cells (0.5%) die each day due to apoptosis.) For an average human child between eight and fourteen years old, each day the approximate lost is 20 to 30 billion cells.[3]
In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis is a highly regulated and controlled process that confers advantages during an organism's life cycle. For example, the separation of fingers and toes in a developing human embryo occurs because cells between the digits undergo apoptosis. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them.[4]
Because apoptosis cannot stop once it has begun, it is a highly regulated process. Apoptosis can be initiated through one of two pathways. In the intrinsic pathway the cell kills itself because it senses cell stress, while in the extrinsic pathway the cell kills itself because of signals from other cells. Weak external signals may also activate the intrinsic pathway of apoptosis.[5] Both pathways induce cell death by activating caspases, which are proteases, or enzymes that degrade proteins. The two pathways both activate initiator caspases, which then activate executioner caspases, which then kill the cell by degrading proteins indiscriminately.
In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in a wide variety of diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer. Some factors like Fas receptors and caspases promote apoptosis, while some members of the Bcl-2 family of proteins inhibit apoptosis.[6]
See also
- ↑ Green D; "Means to an End: Apoptosis and other Cell Death Mechanisms" , ISBN: 978-0-87969-888-1
- ↑ Böhm I, Schild H; "Apoptosis: the complex scenario for a silent cell death" , https://doi.org/10.1016/S1536-1632(03)00024-6
- ↑ Karam JA; "Apoptosis in Carcinogenesis and Chemotherapy" , ISBN: 978-1-4020-9597-9
- ↑ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P; "Molecular Biology of the Cell (textbook)" , pp. 1115 , ISBN: 978-0-8153-4105-5
- ↑ Raychaudhuri S; "A minimal model of signaling network elucidates cell-to-cell stochastic variability in apoptosis" , https://doi.org/10.1371/journal.pone.0011930
- ↑ Elmore S; "Apoptosis: A Review of Programmed Cell Death" , https://doi.org/10.1080/01926230701320337