Mitophagy and Mitochondrial Quality Control in Parkinson's Disease

Dear Colleagues,

One salient feature that underpins the development of neurodegenerative disorders, such as Parkinson’s disease (PD), is the dysregulation of mitochondrial function. Mammalian cells have evolved sophisticated quality control mechanisms to identify, repair, and/or eliminate abnormal and/or dysfunctional mitochondria. Chaperones identify any unstable or abnormal conformations in mitochondrial proteins and often help them to regain their correct conformation Nevertheless, if repair is not an option, the dysregulated protein is degraded. The autophagy–lysosomal system and ubiquitin–proteasome system mediate the selective and targeted degradation of abnormal or aberrant protein fragments. Mitophagy (a specific kind of autophagy) mediates the selective removal of the dysfunctional or abnormal mitochondrion from the cell to prevent the propagation of dysfunctional mitochondria.

Despite the increasing understanding of the molecular counteracting responses toward dysfunctional mitochondria, molecular knowledge regarding the physiological and pathophysiological implications of different protein quality control and mitochondrial quality control pathways are still emerging. This Special Issue aims to cover in-depth manuscripts that provide valuable insights into the different mechanisms of mitochondrial quality control and mitochondrial degradation (mitophagy) in context of Parkinson’s disease, ranging from basic research to translational research. Original research articles, timely reviews, and short communications are welcome.

Dr. Mohamed Eldeeb
Guest Editor

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• protein degradation
• protein quality control
• proteasome
• ubiquitin
• autophagy
• mitophagy
• mitochondrial quality control
• mitochondrial import
• proteolysis
• neurodegeneration