Apoptosis

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Info bulb.pngApoptosis was first described in 1972.[1] The term derives from Greek and is the word used to describe the falling away of leaves, a somewhat poetic comparison to the autumnal process of leaves falling away.

Apoptosis is a form of programmed cell death triggered by various stimuli and regarded as an auto-destruct mechanism. This mechanism is well-conserved against mutation through natural selection. Important as a stop against cancers and essential in development. [2] [3] Affecting apoptosis may be of use in treatment of some cancers [4]


Once triggered, apoptosis involves a co-ordinated and well-regulated dismantlement of the cellular apparatus, leaving cell remnants that are easily phagocytosed by neighbouring cells. The apoptotic cell vanishes without a trace, leaving no chaos in the aftermath of its demise.

In contrast, cell necrosis occurs when toxic stimuli, e.g. heat, mechanical damage and extremes of pH, irretrievably damage the cell, causing uncontrolled cell death, catastrophic cell lysis and inflammation. However programmed necroptosis does occur. A high volume of apoptosis can overwhelm phagocytic capacity and can lead to secondary necrosis, although again the greater understanding of programmed necroptosis and the formation of the ripoptosome might make this an over simplification.

Apoptosis is an energy requiring process, necrosis is not, although this is not true of programmed necroptosis. Leaf fall is an active process. Leaves tend to stay on a tree branch broken off in summer.

Apoptosis Pathways

  1. Extrinsic pathway(s) through cell membrane receptors that can act directly through cytoplasmic caspase or through mitocondrial cytochrome C associated pathways. Both are mediated by a family of enzymes called caspases [5].
  2. Intrinsic pathway through mitochondrial stress signalling leading to DNA fragmentation
  3. DNA damage activating the P53 pathway

Some of the genes involved will be tumour suppressors. Others are autogenes and oncogenes. Indeed isoforms created by alternative splicing of active proteins can have opposite effects.

References

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