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Cell death

From Wikipedia, the free encyclopedia
(Redirected from Cell survival)
For the journal, see Cell Death & Differentiation.

Overview of signal transduction pathways involved in apoptosis

Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part. Apoptosis or Type I cell-death, and 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

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Programmed cell death

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Programmed cell death (PCD) is cell death mediated by an intracellular program.[5][6] PCD is carried out in a regulated process, which usually confers advantage 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 separate. PCD serves fundamental functions during both plant and metazoa (multicellular animals) tissue development.

Apoptosis

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Morphological changes associated with apoptosis

Apoptosis is the processor of programmed cell death (PCD) that may occur in multicellular organisms.[6] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, 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

Certain key proteins primarily employed in the repair of DNA damage can also induce apoptosis when DNA damage exceeds the cell’s repair capability.[8] These dual role proteins protect against proliferation of unstable damaged cells that might lead to cancer.

Autophagy

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Autophagy is cytoplasmic, characterized by the formation of large vacuoles that eat away organelles in a specific sequence prior to the destruction of the nucleus.[9] Macroautophagy, often referred to as autophagy, is a catabolic process that results in the autophagosomic-lysosomal degradation of bulk cytoplasmic contents, abnormal protein aggregates, and excess or damaged organelles. Autophagy is generally activated by conditions of nutrient deprivation but has also been associated with physiological as well as pathological processes such as development, differentiation, neurodegenerative diseases, stress, infection and cancer.

Other variations of PCD

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Other pathways of programmed cell death have been discovered.[10] 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 anoikis, almost identical to apoptosis except in its induction; cornification, a form of cell death exclusive to the eyes; excitotoxicity; ferroptosis, an iron-dependent form of cell death[11] 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).[12] It occurs as a result of repeated stimulation of specific T-cell receptors (TCR) and it helps to maintain the periphery immune tolerance.[13] Therefore, an alteration of the process may lead to autoimmune diseases.[12] In the other words AICD is the negative regulator of activated T-lymphocytes.

Ischemic cell death, or oncosis, is a form of accidental, or passive cell death that is often considered a lethal injury. The process is characterized by mitochondrial swelling, cytoplasm vacuolization, and swelling of the nucleus and cytoplasm.[14]

Mitotic catastrophe is an oncosuppressive mechanism that can lead to cell death that is due to premature or inappropriate entry of cells into mitosis.[15] It is the most common mode of cell death in cancer cells exposed to ionizing radiation and many other anti-cancer treatments.[16]

Immunogenic cell death or immunogenic apoptosis is a form of cell death caused by some cytostatic agents such as anthracyclines, oxaliplatin and bortezomib, or radiotherapy and photodynamic therapy (PDT).[17]

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.[18]

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.[19]

Necrotic cell death

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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. It is the sum of what happens to cells after their deaths.[20] 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.[21] 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.[21] Identification of cell death was previously classified based on morphology, but in recent years switched to molecular and genetic conditions.

See also

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References

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  1. ^ Kierszenbaum A (2012). Histology and Cell Biology – An Introduction to Pathology. Philadelphia: Elsevier Saunders.
  2. ^ Nirmala JG, Lopus M (April 2020). "Cell death mechanisms in eukaryotes". Cell Biology and Toxicology. 36 (2): 145–164. doi:10.1007/s10565-019-09496-2. PMID 31820165.
  3. ^ a b Darzynkiewicz Z, Juan G, Li X, Gorczyca W, Murakami T, Traganos F (January 1997). "Cytometry in cell necrobiology: analysis of apoptosis and accidental cell death (necrosis)". Cytometry. 27 (1): 1–20. doi:10.1002/(sici)1097-0320(19970101)27:1<1::aid-cyto2>3.0.co;2-l. PMID 9500580.
  4. ^ Warnes G, Martins S (March 2011). "Real-time flow cytometry for the kinetic analysis of oncosis". Cytometry. Part A. 79 (3): 181–191. doi:10.1002/cyto.a.21022. PMID 21254392. S2CID 11691981.
  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. doi:10.1371/journal.pgen.0020135. PMC 1626106. PMID 17069462.
  6. ^ a b Green D (2011). Means To An End. New York: Cold Spring Harbor Laboratory Press. ISBN 978-0-87969-887-4.
  7. ^ Bowen ID (April 1993). "Apoptosis or programmed cell death?". Cell Biology International. 17 (4): 365–380. doi:10.1006/cbir.1993.1075. PMID 8318948. S2CID 31016389.
  8. ^ Bernstein C, Bernstein H, Payne CM, Garewal H (June 2002). "DNA repair/pro-apoptotic dual-role proteins in five major DNA repair pathways: fail-safe protection against carcinogenesis". Mutat Res. 511 (2): 145–78. Bibcode:2002MRRMR.511..145B. doi:10.1016/s1383-5742(02)00009-1. PMID 12052432.
  9. ^ 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. Bibcode:1993PNAS...90..980S. doi:10.1073/pnas.90.3.980. PMC 45794. PMID 8430112.;and, for a more recent view, see Bursch W, Ellinger A, Gerner C, Fröhwein U, Schulte-Hermann R (2000). "Programmed cell death (PCD). Apoptosis, autophagic PCD, or others?". Annals of the New York Academy of Sciences. 926 (1): 1–12. Bibcode:2000NYASA.926....1B. doi:10.1111/j.1749-6632.2000.tb05863.x. PMID 11193023. S2CID 27315958.
  10. ^ Kroemer G, Martin SJ (July 2005). "Caspase-independent cell death". Nature Medicine. 11 (7): 725–730. doi:10.1038/nm1263. PMID 16015365. S2CID 8264709.
  11. ^ Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. (May 2012). "Ferroptosis: an iron-dependent form of nonapoptotic cell death". Cell. 149 (5): 1060–1072. doi:10.1016/j.cell.2012.03.042. PMC 3367386. PMID 22632970.
  12. ^ a b Zhang J, Xu X, Liu Y (June 2004). "Activation-induced cell death in T cells and autoimmunity". Cellular & Molecular Immunology. 1 (3): 186–92. PMID 16219166.
  13. ^ Kabelitz D, Janssen O (February 1997). "Antigen-induced death of T-lymphocytes". Frontiers in Bioscience: A Journal and Virtual Library. 2 (4): d61–77. doi:10.2741/a175. PMID 9159213.
  14. ^ "Oncosis". Cell Communication Online Pathfinder Encyclopaedia (COPE). Retrieved 10 August 2010.
  15. ^ Vitale I, Galluzzi L, Castedo M, Kroemer G (June 2011). "Mitotic catastrophe: a mechanism for avoiding genomic instability". Nature Reviews. Molecular Cell Biology. 12 (6): 385–392. doi:10.1038/nrm3115. PMID 21527953. S2CID 22483746.
  16. ^ Ianzini F, Mackey MA (2007). "Mitotic Catastrophe in Apoptosis, Senescence, and Cancer". In Gewirtz DA, Holt SE, Grant S (eds.). Revista Brasileira de Ciências Farmacêuticas. Vol. 44. Humana Press. pp. 73–91. doi:10.1007/978-1-59745-221-2. ISBN 978-1-58829-527-9.
  17. ^ Garg AD, Nowis D, Golab J, Vandenabeele P, Krysko DV, Agostinis P (January 2010). "Immunogenic cell death, DAMPs and anticancer therapeutics: an emerging amalgamation". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer. 1805 (1): 53–71. doi:10.1016/j.bbcan.2009.08.003. PMID 19720113.
  18. ^ Gullett JM, Tweedell RE, Kanneganti TD (April 2022). "It's All in the PAN: Crosstalk, Plasticity, Redundancies, Switches, and Interconnectedness Encompassed by PANoptosis Underlying the Totality of Cell Death-Associated Biological Effects". Cells. 11 (9): 1495. doi:10.3390/cells11091495. PMC 9105755. PMID 35563804.
  19. ^ Brown GC (February 2024). "Cell death by phagocytosis". Nature Reviews. Immunology. 24 (2): 91–102. doi:10.1038/s41577-023-00921-6. PMID 37604896.
  20. ^ Fink SL, Cookson BT (April 2005). "Apoptosis, Pyroptosis, and Necrosis: Mechanistic Description of Dead and Dying Eukaryotic Cells". Infection and Immunity. 73 (4): 1907–1916. doi:10.1128/IAI.73.4.1907-1916.2005. PMC 1087413. PMID 15784530.
  21. ^ a b D'Arcy MS (June 2019). "Cell death: a review of the major forms of apoptosis, necrosis and autophagy". Cell Biology International. 43 (6): 582–592. doi:10.1002/cbin.11137. PMID 30958602. S2CID 102347423.
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