Mitophagy and Mitochondrial Quality Control

Mitochondria are essential for cells that need to maximize ATP production. Neurons in the brain are particularly reliant on mitochondria for their energy needs, which are tremendous due to ATP required to maintain the electrochemical membrane potential that mediates neuronal communication. Yet, mitochondria are a potential threat to cells, as they produce free radicals and reactive oxygen species as byproducts of oxidative phosphorylation. The resulting oxidative stress can damage cell and result in neurodegeneration. Unlike many cells of the body, neurons are not easily replaced by stem cells and must survive with the risk of mitochondrial oxidative stress for decades. Neurons and other cells employ quality control mechanisms to offset potential damage from rogue mitochondria. One such mechanism is mitochondria-selective autophagy (mitophagy), which recognizes rogue mitochondria, engulfs them in augophagosomal membranes, and digests them following fusion with lysosomes. Failure to remove offensive mitochondria is associated with aspects of aging and diseases like Parkinson’s Disease.

Questions About Mitophagy

How do cells recognize a rogue mitochondria from a functional one?

What are the factors that mediate mitophagy?

How does mitophagy differ in different tissue types or during aging?

How is mitophagy regulated?

What is the link between mitophagy and neurodegeneration?

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Mitochondrial Dynamics

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Transcription Factors and Their Targets