細胞死には、necrosis, necroptosis, apoptosisなどの種類がありますが、これらは進化的にどのような関係があるのでしょうか。どのような順番で現れたのか、どの生物種にはどれが存在するのか、おのおのの細胞死の形態は、病態に関与するだけなのか、それとも正常な発生などでも起こっているのか、そのあたりが気になりました。
Although stimulation of the Fas/TNFR receptor family triggers a canonical ‘extrinsic’ apoptosis pathway, we demonstrated that in the absence of intracellular apoptotic signaling it is capable of activating a common nonapoptotic death pathway, which we term necroptosis. (Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury 29 May 2005 Nature Chemical Biology volume 1, pages112–119)
- Complex Pathologic Roles of RIPK1 and RIPK3: Moving Beyond Necroptosis necroptosisの発見者らによる12年後（2017年）のレビュー論文
necroptosisや ferroptosisは病態に関与するものであって、細胞の正常な機能が失われたときに起こる。apoptosisのように生理的な条件でも起こる細胞死とは根本的に異なるという注意を促す論文がありました。
Many cell death forms occur under non-physiological conditions, including necroptosis, ferroptosis and others. In these, an essential cellular function is disrupted, leading to cell loss. The term ‘regulated cell death’ is used to group these cell death forms with apoptosis. However, this is misleading, as it implies that, like apoptosis, these death forms have been evolutionarily selected for their cell-lethal functions, a claim that is unsupported. (Cell death in animal development 2020 Development)
necroptosisと病態との関連のレビュー論文。ネクロプトーシスの制御が失われることが、がんや神経変性、炎症性疾患などに関係しているという主張。
Necroptosis is induced by toll-like receptor, death receptor, interferon, and some other mediators. Shreds of evidence based on a mouse model reveals that deregulation of necroptosis has been found to be associated with pathological conditions like cancer, neurodegenerative diseases, and inflammatory diseases.
進化的な視点によるレビュー論文
How and when necroptosis is triggered under physiological conditions therefore remains a persistent question.
the role of necroptosis in the response to viral infection
why the necroptotic pathway has been favored during evolution
（Controlled detonation: evolution of necroptosis in pathogen defense Michelle Brault, Andrew Oberst First published: 20 December 2016）