The bioenergetic status of a cell plays a critical role in determining its ability to survive. Cells unable to maintain sufficient ATP production to support essential cellular processes die passively by necrosis. In contrast, apoptosis is an organized and energy-dependent form of cell death. Recently, genes involved in bioenergetic control and/or mitochondrial function have been implicated in the regulation of apoptosis. The purpose of this meeting is to define the role of bioenergetics in determining a cell's susceptibility to apoptosis. Among the issues to be considered are: the contribution of metabolic regulators (Akt, PGC-1, and HIF-1a) to mitochondrial function and apoptotic susceptibility, the role of bioenergetic sensing pathways (AMPK, TOR, autophagy) in modulating apoptotic sensitivity, and the determination of how mitochondrial function influences the contributions of calcium, oxidative stress, and Bcl-2 family proteins to apoptotic regulation. The meeting will focus on how these relationships may contribute to understanding the pathogenesis and improving the treatment of a wide variety of disorders including neurodegenerative syndromes, cancer, and cardiovascular disease. This symposium will consider the role cellular metabolism plays in regulating cell survival/death. Recent evidence suggests that genes which control a cell's production of ATP are also critical regulators of programmed cell death (apoptosis). Understanding the relationships between metabolism and apoptosis may lead to novel approaches for the prevention and/or treatment of cancer and degenerative disorders.
