Necroptosis
DENekroptose
Necroptosis is a controlled but messy way for your cells to die. Unlike tidy apoptosis, the cell bursts open, but it still follows a defined molecular script. The key players are two kinases, RIPK1 and RIPK3, and a pore-forming protein, MLKL. When apoptosis is blocked or overwhelmed, RIPK3 switches on MLKL, which clusters and punches into the cell membrane. The cell ruptures and spills its contents, including alarm signals called DAMPs (damage-associated molecular patterns). Because of those DAMPs, necroptosis is inherently inflammatory. It can be set off by death-receptor signals, viral sensors, and toll-like receptors. Growing evidence ties it to age-related problems like neurodegeneration, damage from lost blood flow, and inflammatory bowel disease, though how much it drives normal aging (versus acute disease) is still being worked out.
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Sources
- Cho YS, Challa S, Moquin D, Genga R, Ray TD, Guildford M, Chan FK. (2009). Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. *Cell*doi:10.1016/j.cell.2009.05.037
- Weinlich R, Oberst A, Beere HM, Green DR. (2016). Necroptosis in development, inflammation and disease. *Nature Reviews Molecular Cell Biology*doi:10.1038/nrm.2016.149