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Journal Article

Mechanisms of mitochondria and autophagy crosstalk

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Rambold,  Angelika
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Rambold, A., & Lippincott-Schwarz, J. (2011). Mechanisms of mitochondria and autophagy crosstalk. Cell Cycle, 10, 4032-4038. doi:10.4161/cc.10.23.18384.


Cite as: http://hdl.handle.net/21.11116/0000-0005-C441-4
Abstract
Autophagy is a cellular survival pathway that recycles intracellular components to compensate for nutrient depletion and ensures the appropriate degradation of organelles. Mitochondrial number and health are regulated by mitophagy, a process by which excessive or damaged mitochondria are subjected to autophagic degradation. Autophagy is thus a key determinant for mitochondrial health and proper cell function. Mitophagic malfunction has been recently proposed to contribute to progressive neuronal loss in Parkinson's disease. In addition to autophagy's significance in mitochondrial integrity, several lines of evidence suggest that mitochondria can also substantially influence the autophagic process. The mitochondria's ability to influence and be influenced by autophagy places both elements (mitochondria and autophagy) in a unique position where defects in one or the other system could increase the risk to various metabolic and autophagic related diseases.