@article {47662,
	title = {Mechanisms of mitochondria and autophagy crosstalk.},
	journal = {Cell cycle (Georgetown, Tex.)},
	volume = {10},
	year = {2011},
	month = {2011 Dec 1},
	pages = {4032-8},
	abstract = {<p>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{\textquoteright}s disease. In addition to autophagy{\textquoteright}s significance in mitochondrial integrity, several lines of evidence suggest that mitochondria can also substantially influence the autophagic process. The mitochondria{\textquoteright}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.</p>
},
	keywords = {Animals, Apoptosis, Autophagy, DNA Replication, DNA, Mitochondrial, Humans, Mammals, Metabolic Diseases, Microtubule-Associated Proteins, Mitochondria, Mitochondrial Membranes, Mitochondrial Proteins, Stress, Physiological},
	issn = {1551-4005},
	doi = {10.4161/cc.10.23.18384},
	author = {Rambold, Angelika S and Lippincott-Schwartz, Jennifer}
}
