Cell death

Source: Wikipedia, the free encyclopedia.
For the journal, see Cell Death & Differentiation.
Overview of signal transduction pathways involved in apoptosis

Cell death is the event of a

autophagy or Type II cell-death are both forms of programmed cell death, while necrosis is a non-physiological process that occurs as a result of infection or injury.[1]

The term "cell necrobiology" has been used to describe the life processes associated with morphological, biochemical, and molecular changes which predispose, precede, and accompany cell death, as well as the consequences and tissue response to cell death.[2] The word is derived from the Greek νεκρό meaning "death", βìο meaning "life", and λόγος meaning "the study of". The term was initially coined to broadly define investigations of the changes that accompany cell death, detected and measured by multiparameter flow- and laser scanning- cytometry.[3] It has been used to describe the real-time changes during cell death, detected by flow cytometry.[4]

Types

Programmed cell death

Programmed cell death (PCD) is cell death mediated by an intracellular program.

metazoa
(multicellular animals) tissue development.

Apoptosis

Morphological changes associated with apoptosis

chromatin condensation, and chromosomal DNA fragmentation. It is now thought that – in a developmental context – cells are induced to positively commit suicide whilst in a homeostatic context; the absence of certain survival factors may provide the impetus for suicide. There appears to be some variation in the morphology and indeed the biochemistry of these suicide pathways; some treading the path of "apoptosis", others following a more generalized pathway to deletion, but both usually being genetically and synthetically motivated. There is some evidence that certain symptoms of "apoptosis" such as endonuclease activation can be spuriously induced without engaging a genetic cascade, however, presumably true apoptosis and programmed cell death must be genetically mediated. It is also becoming clear that mitosis and apoptosis are toggled or linked in some way and that the balance achieved depends on signals received from appropriate growth or survival factors.[7]

Example events in autophagy

Autophagy

Autophagy is

stress, infection and cancer
.

Other variations of PCD

Other pathways of programmed cell death have been discovered.[9] Called "non-apoptotic programmed cell-death" (or "caspase-independent programmed cell-death"), these alternative routes to death are as efficient as apoptosis and can function as either backup mechanisms or the main type of PCD.

Some such forms of programmed cell death are

cornification, a form of cell death exclusive to the eyes; excitotoxicity; ferroptosis, an iron-dependent form of cell death[10] and Wallerian degeneration
.

Plant cells undergo particular processes of PCD similar to autophagic cell death. However, some common features of PCD are highly conserved in both plants and metazoa.

Activation-induced cell death (AICD) is a programmed cell death caused by the interaction of Fas receptor (Fas, CD95)and Fas ligand (FasL, CD95 ligand).[11] It occurs as a result of repeated stimulation of specific T-cell receptors (TCR) and it helps to maintain the periphery immune tolerance.[12] Therefore, an alteration of the process may lead to autoimmune diseases.[11]
In the other words AICD is the negative regulator of activated T-lymphocytes.

swelling, cytoplasm vacuolization, and swelling of the nucleus and cytoplasm.[13]

Mitotic catastrophe is an oncosuppressive mechanism that can lead to cell death that is due to premature or inappropriate entry of cells into mitosis.[14] It is the most common mode of cell death in cancer cells exposed to ionizing radiation and many other anti-cancer treatments.[15]

radiotherapy and photodynamic therapy (PDT).[16]

Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response in myeloid cells.[3]

PANoptosis is a unique inflammatory cell death pathway that integrates components from other cell death pathways. The totality of biological effects in PANoptosis cannot be individually accounted for by pyroptosis, apoptosis, or necroptosis alone. PANoptosis is regulated by multifaceted macromolecular complexes termed PANoptosomes.[17]

Phagoptosis is cell death resulting from a live cell being phagocytosed (i.e. eaten) by another cell (usually a phagocyte), resulting in death and digestion of the engulfed cell. Phagoptosis can occur to cells that are pathogenic, cancerous, aged, damaged or excess to requirements.[18]

Necrotic cell death

Necrosis is cell death where a cell has been badly damaged through external forces such as trauma or infection and occurs in several different forms. In necrosis, a cell undergoes swelling, followed by uncontrolled rupture of the cell membrane with cell contents being expelled. These cell contents often then go on to cause inflammation in nearby cells.[19] A form of programmed necrosis, called necroptosis, has been recognized as an alternative form of programmed cell death. It is hypothesized that necroptosis can serve as a cell-death backup to apoptosis when the apoptosis signaling is blocked by endogenous or exogenous factors such as viruses or mutations. Necroptotic pathways are associated with death receptors such as the tumor necrosis factor receptor 1.[19] Identification of cell death was previously classified based on morphology, but in recent years switched to molecular and genetic conditions.

See also

References

  1. ^ Kierszenbaum A (2012). Histology and Cell Biology – An Introduction to Pathology. Philadelphia: Elsevier Saunders.
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  5. ^ Engelberg-Kulka H, Amitai S, Kolodkin-Gal I, Hazan R (October 2006). "Bacterial programmed cell death and multicellular behavior in bacteria". PLOS Genetics. 2 (10): e135.
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  8. ^ Schwartz LM, Smith SW, Jones ME, Osborne BA (February 1993). "Do all programmed cell deaths occur via apoptosis?". Proceedings of the National Academy of Sciences of the United States of America. 90 (3): 980–984.
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  9. ^ Kroemer G, Martin SJ (July 2005). "Caspase-independent cell death". Nature Medicine. 11 (7): 725–730.
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  13. ^ "Oncosis". Cell Communication Online Pathfinder Encyclopaedia (COPE). Retrieved 10 August 2010.
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