Necrosis Research Paper

Necrosis occurs as a result of external injury due to cellular injury, bacterial toxin or trauma to a particular area of the body. Necrosis differs from apoptosis in a couple of ways. First, the morphological changes that a cell undergoes are different in necrosis compared to apoptosis. Secondly, apoptosis is highly regulated, however, necrosis is unregulated. The morphological changes that a cell undergoes during necrosis are the swelling of the cytoplasm, irreversible damage to the plasma membrane, organelle breakdown and the breakdown of the nucleus. (Majno) The breakdown of the nucleus happens randomly by DNAse. Necrosis is initiated because the damage to the plasma membrane leaks intracellular contents to the extracellular environment. This leakage activates many different …show more content…
There are many death receptors that promote a cell to undergo necrosis. One key player in the result of necrotic cell death is Receptor Interacting Serine/Threonine Protein Kinase 1 (RIP1) and Receptor Interacting Serine/Threonine Protein Kinase 3 (RIP3) which when combined they make a necrosome. (Jog) Tumor Necrosis Factor Receptor Type 1 - associated Death Domain (TRADD) is required for the recruitment of RIP1 and RIP3 to TNFR1. RIP1 activates Tumor Necrosis Factor alpha necrosis and its phosphorylating activity activates leads to signaling cascades in other necrotic death receptors such as Fas or Tumor Necrosis Factor Receptor 1 (TNFR1). TNFR1 is activated by the binding of a ligand, such as an initiator caspase, which leads to a conformational change of the receptor. RIP1 activates Nuclear Factor - kappa light chain enhancer of activated B cells (NF-kB.) Caspase 8 can inhibit this pathway from occurring and leads to anti-necrosis or anti-apoptotic pathway. The NF-kB pathway can be activated by TNFR1 but it can also be activated by a variety of bacterial toxins, pathogens or