Mitophagy provides a highly precise means to degrade suboptimal or damaged mitochondria via autophagy. Mitochondria destined for degradation are tagged with phosphoubiquitin, and various cytosolic ATG proteins are activated to begin the degradation process. The process of mitophagy is primarily regulated by two enzymes: PINK1 kinase and Parkin E3 ligase. Loss of function mutations in these recessive genes have been linked to familial Parkinson’s disease, and so much attention has been given to understanding PINK1/Parking-mediated mitophagy.
However, recent discoveries have shown that there are mechanisms of inducing mitophagy independently of this pathway. Hypoxia and iron chelation are two such mechanisms, and recent studies have also highlighted the role of inter-organelle membrane contact sites in regulating mitochondrial function. There are many unanswered questions regarding the exact mechanisms by which PINK1/Parkin-independent mitophagy is achieved, as well as their specific physiological role.
This research topic aims to expand our current understanding of mitophagy, with express interest in non-PINK1/Parkin mechanisms of regulating this process. Original research articles, method articles, review articles, perspectives, and opinion articles broadly on the topic of mitophagy will all be considered.
Topics of interest include but are not limited to:
- Development of new reporters for better quantitative and qualitative measurement of mitophagy
- Identification of novel pathways that modulate mitophagy
- Novel links between metabolic pathways, mitochondrial pathways, and mitophagy
- The role of membrane compartments and/or organelle contact sites in facilitating mitophagy
- Screening of novel compounds that facilitate mitophagy
Mitophagy provides a highly precise means to degrade suboptimal or damaged mitochondria via autophagy. Mitochondria destined for degradation are tagged with phosphoubiquitin, and various cytosolic ATG proteins are activated to begin the degradation process. The process of mitophagy is primarily regulated by two enzymes: PINK1 kinase and Parkin E3 ligase. Loss of function mutations in these recessive genes have been linked to familial Parkinson’s disease, and so much attention has been given to understanding PINK1/Parking-mediated mitophagy.
However, recent discoveries have shown that there are mechanisms of inducing mitophagy independently of this pathway. Hypoxia and iron chelation are two such mechanisms, and recent studies have also highlighted the role of inter-organelle membrane contact sites in regulating mitochondrial function. There are many unanswered questions regarding the exact mechanisms by which PINK1/Parkin-independent mitophagy is achieved, as well as their specific physiological role.
This research topic aims to expand our current understanding of mitophagy, with express interest in non-PINK1/Parkin mechanisms of regulating this process. Original research articles, method articles, review articles, perspectives, and opinion articles broadly on the topic of mitophagy will all be considered.
Topics of interest include but are not limited to:
- Development of new reporters for better quantitative and qualitative measurement of mitophagy
- Identification of novel pathways that modulate mitophagy
- Novel links between metabolic pathways, mitochondrial pathways, and mitophagy
- The role of membrane compartments and/or organelle contact sites in facilitating mitophagy
- Screening of novel compounds that facilitate mitophagy