作者: Agnieszka K. Biala , Lorrie A. Kirshenbaum
DOI: 10.1016/J.TCM.2014.08.002
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摘要: To date, one of the most intriguing and compelling concepts to impact contemporary cell biology is notion that fate “programmed” or genetically controlled. Indeed, regulation crucial for embryonic development, tissue homeostasis. Given importance removing damaged irreversibly injured cells from body, it not surprising defects in regulatory mechanisms govern death and/or survival more generally have been implicated a number human pathologies including cancer, neurodegenerative diseases, cardiac failure. Several processes involved through apoptosis, necrosis, autophagy are commonly linked actions certain Bcl-2 proteins act on mitochondrion. For example, protein Beclin-1 actively clearance mitochondria via mitophagy, while other such as Bax/Bak can initiate apoptosis necrotic signaling pathways. The overlapping redundant nature these highlights their evolutionary regulating during normal disease states. Here, we explore interrelationship between pathways cellular effectors influence fate.