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A discussion of every disease caused by modification of the various apoptotic pathways would be impractical, but the concept overlying each one is the same: The normal functioning of the pathway has been disrupted in such a way as to impair the ability of the cell to undergo normal apoptosis.
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
Once the apoptosome was established as the procaspase-9 activator, mutations within this pathway became an important research area. Some examples include human leukemia cells, ovarian cancer and viral infections. [8] [9] [10] Current research areas for this pathway will be discussed in further detail. There are hidden routes for cell death as ...
Efferocytosis triggers specific downstream intracellular signal transduction pathways, for example resulting in anti-inflammatory, anti-protease and growth-promoting effects. Conversely, impaired efferocytosis has been linked to autoimmune disease and tissue damage.
Even after the initial cause of the necrosis has been halted, the necrotic tissue will remain in the body. The body's immune response to apoptosis, which involves the automatic breaking down and recycling of cellular material, is not triggered by necrotic cell death due to the apoptotic pathway being disabled. [29]
It is proposed that both pyroptosis and necroptosis may act as defence systems against pathogens when apoptotic pathways are blocked. [ citation needed ] Summary of the different morphologies, mechanisms and outcomes of three most well-characterized forms of cell death (apoptosis, pyroptosis, and necrosis) [ 10 ] [ 6 ] [ 17 ]
Apoptosis Inducing Factor (AIF) is a protein that triggers chromatin condensation and DNA fragmentation in a cell in order to induce programmed cell death. The mitochondrial AIF protein was found to be a caspase-independent death effector that can allow independent nuclei to undergo apoptotic changes.
Primarily, apoptosis is dependent on the caspase pathway activated by cytochrome c release, while the parthanatos pathway is able to act independently of caspase. [8] Furthermore, unlike apoptosis, parthanatos causes large scale DNA fragmentation (apoptosis only produces small scale fragmentation) and does not form apoptotic bodies. [25]