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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Therapeutic potential of autophagy-enhancing agents in Parkinson’s disease

Fig. 1

Molecular regulation of macroautophagy and targets for pharmacological stimulation of the autophagy-lysosomal pathway. Situations of amino acid deprivation and low amounts of energy, detected by AMPK, can lead to the inhibition of mTORC1, resulting in the initiation of autophagy via activation of the ULK1-FIP200-Atg13 complex. In this situation, TFEB is dephosphorylated and translocates to the cell nucleus where it binds to ATGs to activate de novo gene transcription. Deprivation of growth factors or insulin results in reduced activation of the PI3K Class 1 complex, which promotes the formation of autophagosomes via activation of the Beclin-1-VSP34 complex. A final mTOR-independent pathway, involving the generation of IP3, acts as a negative regulator of autophagy. A number of autophagy-enhancing agents, shown in red, is yet available, allowing to act at different levels of the autophagy-lysosomal pathway

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