MATHEMATICAL MODELING AND SIMULATION OF APOPTOSIS AND NITRIC OXIDE EFFECTS

TL;DRAbstract

Apoptosis, or programmed cell death, is a process of crucial importance for maintaining a homeostatic balance between cell proliferation and death. In the present study a new mathematical model is presented that draws attention to the possible occurrence of bistability in mitochondria-dependent apoptotic pathways, as well as a transition from bistable to monostable behavior -either apoptotic or cytoprotective, under well-defined conditions. Bistability is proposed to be conferred by positive feedback loops that enhance caspase-3 activation pathways through mitochondria and by kinetic cooperativity in the formation of an apoptosome complex. It essentially ensures that cells will not die in the presence of relatively small pro-apoptotic effects, but will undergo apoptosis when perturbing conditions or levels of pro-apoptotic agents exceed certain threshold values. The passage from bistable to monostable cytoprotective behavior i.e., resistance to apoptosis, may be induced by decreasing t

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