Editing Cell death (section)

==== Apoptosis ====
[[File:Apoptotic_cell_disassembly.png|thumb|Morphological changes associated with apoptosis]]
[[Apoptosis]] is the processor of programmed cell death (PCD) that may occur in [[multicellular organisms]].<ref name="Green_2011" /> [[Biochemical]] events lead to characteristic cell changes ([[Morphology (biology)|morphology]]) and death. These changes include [[Bleb (cell biology)|blebbing]], cell shrinkage, [[Cell nucleus|nuclear]] fragmentation, [[chromatin condensation]], and [[Chromosome|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.<ref name="Apoptosis or programmed cell death?2">{{cite journal | vauthors = Bowen ID | title = Apoptosis or programmed cell death? | journal = Cell Biology International | volume = 17 | issue = 4 | pages = 365–380 | date = April 1993 | pmid = 8318948 | doi = 10.1006/cbir.1993.1075 | s2cid = 31016389 }}</ref>
[[File:Autophagy.jpg|thumb|Example events in autophagy]]
Certain key proteins primarily employed in the [[DNA repair|repair of DNA damage]] can also induce apoptosis when [[DNA damage (naturally occurring)|DNA damage]] exceeds the cell’s repair capability.<ref>{{cite journal |vauthors=Bernstein C, Bernstein H, Payne CM, Garewal H |title=DNA repair/pro-apoptotic dual-role proteins in five major DNA repair pathways: fail-safe protection against carcinogenesis |journal=Mutat Res |volume=511 |issue=2 |pages=145–78 |date=June 2002 |pmid=12052432 |doi=10.1016/s1383-5742(02)00009-1 |bibcode=2002MRRMR.511..145B |url=}}</ref>   These dual role proteins protect against proliferation of unstable damaged cells that might lead to cancer.