Is death a living being?

Abdelrazak Mansour Ali 1, *, Radwa Abdelrazak Ali 2 and Ahmed Abdelrazak Ali 3

1 Department of Pediatrics, Al-Azhar University, Egypt.
2 Department of research. National Institute of Health, USA.
3 Department of Information system, Virginia Commonwealth University, USA.
 
Review
International Journal of Science and Technology Research Archive, 2023, 05(02), 134–141​​.
Article DOI: 10.53771/ijstra.2023.5.2.0294
Publication history: 
Received on 28 October 2023; revised on 18 December 2023; accepted on 21 December 2023
 
Abstract: 
The death process begins with the loss of function of one or more of the three classic vital organs: the heart, the brain, and/or the lungs. Failure to resuscitate the function of the affected primary organ leads to the cessation of the function of other organs. The cell carries death factors or elements such as caspases and some mitochondrial secretions - At the same time the mitochondria represent the basic source of energy and life in the cell. Death occurs only when activating the molecules and factors of cell annihilation. Apoptosis is a type of cell death mechanism, controlled by interactions between several molecules - and is responsible for removing unwanted cells from the body. Apoptosis can be induced by signals from inside the cell or by death signals coming from outside the cell via cosmic energy waves. Caspases are cysteine aspartate-specific proteases that are essential for the initiation and execution of apoptosis. As one of the initiator and executor caspases, caspase-2 is the most evolutionally conserved caspase, exerting both apoptotic and non-apoptotic functions. Caspases also have a role in inflammation, whereby they directly process proinflammatory cytokines such as pro-IL1β. These are signaling molecules that allow recruitment of immune cells to an infected cell or tissue. In addition to apoptosis, caspases play a role in necroptosis, pyroptosis, and autophagy, which are non-apoptotic cell death processes. Mitochondria coordinate cell stress responses, such as autophagy, and control nonapoptotic cell death routines, such as regulated necrosis. Mitochondrial permeabilization leads to release of these proteins, which then interfere with the IAP-inhibition of caspases, resulting in potentiation of cell death. Initiators of mitochondrial-driven inflammation include the release of mitochondrial dsRNA and mt DNA thereby initiating type I interferons. It is concluded that mitochondria not only power the metabolic cell activities with energy but also power the cell death with both energy and signaling molecules denoting that cell death is an active living being.
 
Keywords: 
Cell; Death; Apoptosis; Caspases; Mitochondrial
 
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