Macroautophagy, for simplicity frequently called autophagy, is a mechanism used by cells to survive periods of starvation by degrading cytoplasmic components and releasing muchneeded metabolites and energy. In so doing, autophagy also achieves another feat: removal of dysfunctional and toxic proteins and protein aggregates, as well as entire organelles, such as functionally impaired mitochondria. Therefore up-regulation of autophagy is now considered to be of potential therapeutic benefit in numerous diseases, including neurodegenerative conditions resulting from accumulation of misfolded, intracytoplasmic, aggregate-prone proteins. This article discusses a complex network of signalling pathways upstream of autophagy and potential targets that may allow precise and efficient control of autophagy for therapeutic purposes.

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