
In contrast to the "programmed" nature of apoptosis and autophagy, necrotic cell death has always been believed to be a random, uncontrolled process that leads to the "accidental" death of the cell. This dogma, however, is being challenged and the concept of necrosis also being "programmed" is gaining ground. In particular, mitochondria appear to play a pivotal role in the mediation of programmed necrosis. The purpose of this review, therefore, is to appraise the current concepts regarding the signaling mechanisms of programmed necrosis, with specific attention to the contribution of mitochondria to this process.
reactive oxygen species, Bcl2 proteins, Calpain, Physiology, necrosis, Mitochondria, PARP, mitochondria, Necrosis, RIP kinases, physiology, QP1-981, Reactive Oxygen Species
reactive oxygen species, Bcl2 proteins, Calpain, Physiology, necrosis, Mitochondria, PARP, mitochondria, Necrosis, RIP kinases, physiology, QP1-981, Reactive Oxygen Species
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| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
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