Apoptosis

Apoptosis
An etoposide-treated DU145 prostate cancer cell exploding into a cascade of apoptotic bodies. The sub images were extracted from a 61-hour time-lapse microscopy video, created using quantitative phase-contrast microscopy. The optical thickness is color-coded. With increasing thickness, color changes from gray to yellow, red, purple and finally black.
See the video at The Cell: An Image Library
Identifiers
MeSHD017209
Anatomical terminology

Apoptosis (from Ancient Greek: ἀπόπτωσις, romanized: apóptōsis, lit. 'falling off') 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 50 to 70 billion cells each day due to apoptosis.[a] For the average human child between 8 and 14 years old, each day the approximate loss is 20 to 30 billion cells.[4]

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.[5]

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.[6] 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.[7]

  1. ^ Green D (2011). Means to an End: Apoptosis and other Cell Death Mechanisms. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press. ISBN 978-0-87969-888-1. Archived from the original on 2020-07-26. Retrieved 2020-05-25.
  2. ^ Böhm I, Schild H (2003). "Apoptosis: the complex scenario for a silent cell death". Mol Imaging Biol. 5 (1): 2–14. doi:10.1016/S1536-1632(03)00024-6. PMID 14499155.
  3. ^ Alberts, p. 2.
  4. ^ Karam JA (2009). Apoptosis in Carcinogenesis and Chemotherapy. Netherlands: Springer. ISBN 978-1-4020-9597-9.
  5. ^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2008). "Chapter 18 Apoptosis: Programmed Cell Death Eliminates Unwanted Cells". Molecular Biology of the Cell (textbook) (5th ed.). Garland Science. p. 1115. ISBN 978-0-8153-4105-5.
  6. ^ Raychaudhuri S (August 2010). "A minimal model of signaling network elucidates cell-to-cell stochastic variability in apoptosis". PLOS ONE. 5 (8): e11930. arXiv:1009.2294. Bibcode:2010PLoSO...511930R. doi:10.1371/journal.pone.0011930. PMC 2920308. PMID 20711445.
  7. ^ Elmore S (June 2007). "Apoptosis: A Review of Programmed Cell Death". Toxicologic Pathology. 35 (4): 495–516. doi:10.1080/01926230701320337. PMC 2117903. PMID 17562483.


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