Differences of Key Proteins between Apoptosis and Necroptosis

Abstract

Many different types of programmed cell death (PCD) have been identified, including apoptosis and necroptosis. Apoptosis is a type of cell death that is controlled by various genes. It is in charge of eliminating aberrant cells such as cancer cells, replenishing normal cells, and molding the body as it develops. Necroptosis is a type of programmed cell death that combines necrosis and apoptosis. In other words, it takes on a necrotic appearance, although cells die in a controlled manner. Various investigations of these two pathways have revealed that caspase-8, receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3 are crucial proteins in charge of the switching between these two pathways, resulting in the activation or inhibition of necroptosis. In this review, we have summarized the key proteins between apoptosis and necroptosis.

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“…Cellular necrosis is characterized by cell swelling, membrane rupture, and random degradation of DNA. In contrast, cellular apoptosis involves dense chromatin, formation of DNA fragments, cytoplasmic foam, and apoptotic bodies ( Park et al, 2021a ; Moujalled et al, 2021 ; Saleem, 2021 ). Apoptosis is crucial in ischemic injury and is the primary form of delayed neuronal death after cerebral ischemia ( Mitsios et al, 2007 ; Radak et al, 2017 ; Uzdensky, 2019 ).…”

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“…When a cell stops growing and dividing, it enters apoptosis, a sort of cell death [ 55 ]. Within physiological conditions, in other words, apoptosis ( Figure 2 ) is a critical mechanism that results in the eradication of unwanted cells [ 27 ].…”

“…Caspase-8 and caspase-10 can BID shortened BID in the extrinsic route. The tBID (to be decided or to be determined) activates BAK (BCL2-antagonist/killer 1) and BAX (Bcl-2-associated X protein) [ 55 ]. Inherent lethal stimuli can activate BAX and BAK via stimulating BH3-only proteins.…”

“…As a result, the FAS death effector domain becomes visible, which can be linked to the adaptor protein FAS-associated death domain (FADD) [ 93 ]. Procaspase-8 and procaspase-10 can bind to this domain, cleaving them to activate caspase-8 and caspase-10, which subsequently activate caspase-3 and caspase-7 as effector caspases, breaking the target protein and producing apoptosis [ 55 ].…”

“…Apoptosis is also induced by GL-V9 in human breast cancer cell lines [ 96 ]. By reducing miR-27a expression, isoliquiritigenin, a flavonoid, can also block melanoma cells from growing and migrating [ 55 , 91 ].…”