50:, mitochondrial condensation, chromatin clumping, and cytoplasmic bleb formation. Oncosis refers to a series of cellular reactions following injury that precedes cell death. The process of oncosis is divided into three stages. First, the cell becomes committed to oncosis as a result of damage incurred to the plasma membrane through toxicity or ischemia, resulting in the leak of ions and water due to ATP depletion. The ionic imbalance that occurs subsequently causes the cell to swell without a concurrent change in membrane permeability to reverse the swelling. In stage two, the reversibility threshold for the cell is passed and the cell becomes committed to cell death. During this stage the membrane becomes abnormally permeable to
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or neighboring cells due to size decrease. The phagocytic disposal of apoptotic cells prevents the release of cellular debris that could induce an inflammatory response in neighboring cells. In opposition, the leakage of cellular content associated with membrane disruption in oncosis often incites an
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within the compromised cell membrane. The lack of ion transport at the cell membrane leads to an accumulation of sodium and chloride ions within the cell with a concurrent water influx, contributing to the hallmark cellular swelling of oncosis. As with apoptosis, oncosis has been shown to be
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Scarabelli, T. M., Knight, R., Stephanou, A., Townsend, P., Chen-Scarabelli, C., Lawrence, K., Gottlieb, R., Latchman, D., & Narula, J. (2006). Clinical implications of apoptosis in ischemic myocardium. Current problems in cardiology, 31(3),
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and intracellular ATP levels, initiating the oncotic pathway. The anti-apoptotic gene product Bcl-2 is not an active inhibitor of UCP-2 initiated cell death, further distinguishing oncosis and apoptosis as distinct cellular death mechanisms.
138:. Oligonuclosomal DNA fragmentation is initiated by caspase-activated deoxyribonuclease following caspase-3 mediated cleavage of the enzyme’s inhibitor, ICAD. In contrast, the oncotic pathway has been shown to be caspase-3 independent.
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Yamamoto, N., Smith, M. W., Maki, A., Berezesky, I. K., & Trump, B. F. (1994). Role of cytosolic Ca2+ and protein kinases in the induction of the hsp70 gene. Kidney
International, 45(4), 1093-1104.
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Yamamoto, N., Smith, M. W., Maki, A., Berezesky, I. K., & Trump, B. F. (1994). Role of cytosolic Ca2+ and protein kinases in the induction of the hsp70 gene. Kidney
International, 45(4), 1093-1104.
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Enari, M., Sakahira, H., Yokoyama, H., Okawa, K., Iwamatsu, A., & Nagata, S. (1998). A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD. Nature, 391(6662), 43-50.
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Mills, E. M., Xu, D., Fergusson, M. M., Combs, C. A., Xu, Y., & Finkel, T. (2002). Regulation of cellular oncosis by uncoupling protein 2. Journal of
Biological Chemistry, 277(30), 27385-27392.
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Mills, E. M., Xu, D., Fergusson, M. M., Combs, C. A., Xu, Y., & Finkel, T. (2002). Regulation of cellular oncosis by uncoupling protein 2. Journal of
Biological Chemistry, 277(30), 27385-27392.
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Earnshaw, W. C., Martins, L. M., & Kaufmann, S. H. (1999). Mammalian caspases: structure, activation, substrates, and functions during apoptosis. Annual review of biochemistry, 68(1), 383-424.
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The primary determinant of cell death occurring via the oncotic or apoptotic pathway is cellular ATP levels. Apoptosis is contingent upon ATP levels to form the energy dependent
145:. A distinct biochemical event only seen in oncosis is the rapid depletion of intracellular ATP. The lack of intracellular ATP results in a deactivation of sodium and potassium
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inflammatory response in neighboring tissue, causing further cellular injury. Additionally, apoptosis and the degradation of intracellular organelles is mediated by
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was introduced as the process involves the affected cell(s) swelling to an abnormally large size in known models. This is thought to be caused by failure of the
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Weerasinghe, Priya, and L. Maximilian Buja. "Oncosis: an important non-apoptotic mode of cell death." Experimental and molecular pathology 93.3 (2012): 302-308.
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Weerasinghe, Priya, and L. Maximilian Buja. "Oncosis: an important non-apoptotic mode of cell death." Experimental and molecular pathology 93.3 (2012): 302-308.
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Weerasinghe, Priya, and L. Maximilian Buja. "Oncosis: an important non-apoptotic mode of cell death." Experimental and molecular pathology 93.3 (2012): 302-308.
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Weerasinghe, Priya, and L. Maximilian Buja. "Oncosis: an important non-apoptotic mode of cell death." Experimental and molecular pathology 93.3 (2012): 302-308.
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Weerasinghe, Priya, and L. Maximilian Buja. "Oncosis: an important non-apoptotic mode of cell death." Experimental and molecular pathology 93.3 (2012): 302-308.
58:, indicating membrane compromise. The final stage is cell death and removal of the cell via phagocytosis mediated by an inflammatory response.
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Majno, G., & Joris, I. (1995). Apoptosis, oncosis, and necrosis. An overview of cell death. The
American journal of pathology, 146(1), 3.
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Eguchi Y, Shimizu S and
Tsujimoto Y (1997) Intracellular ATP levels determine cell death fate by apoptosis or necrosis. Cancer Res. in press
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Eguchi Y, Shimizu S and
Tsujimoto Y (1997) Intracellular ATP levels determine cell death fate by apoptosis or necrosis. Cancer Res. in press
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Eguchi Y, Shimizu S and
Tsujimoto Y (1997) Intracellular ATP levels determine cell death fate by apoptosis or necrosis. Cancer Res. in press
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function. Apoptosis, or programmed cell death involves a series of cell shrinking processes, beginning with cell size reduction and
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Ren, Y., & Savill, J. (1998). Apoptosis: the importance of being eaten. Cell Death & Differentiation, 5(7), 563-568.
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Ren, Y., & Savill, J. (1998). Apoptosis: the importance of being eaten. Cell Death & Differentiation, 5(7), 563-568.
154:. An increase in UCP-2 levels leads to a rapid decrease in mitochondrial membrane potential, reducing mitochondrial
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are distinct processes of cellular death. Oncosis is characterized by cellular swelling caused by a failure in
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depletion within the cell leading to impairment of ionic pumps, cell swelling, clearing of the
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genetically programmed and dependent on expression levels of uncoupling protein-2 (UCP-2) in
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is the accepted name of the process, the alternative name of
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95:Friedrich Daniel von Recklinghausen
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134:activation, particularly
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78:ionic pumps. The name
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44:endoplasmic reticulum
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127:macrophages
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136:caspase-3
107:apoptosis
66:Although
62:Etymology
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115:pyknosis
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