@article {26973,
	title = {Mitochondria, autophagy and age-associated neurodegenerative diseases: New insights into a complex interplay},
	journal = {Biochim Biophys Acta},
	volume = {1847},
	number = {11},
	year = {2015},
	note = {Lionaki, EiriniMarkaki, MariaPalikaras, KonstantinosTavernarakis, NektariosengResearch Support, Non-U.S. Gov{\textquoteright}tReviewNetherlandsBiochim Biophys Acta. 2015 Nov;1847(11):1412-23. doi: 10.1016/j.bbabio.2015.04.010. Epub 2015 Apr 24.},
	month = {Nov},
	pages = {1412-23},
	edition = {2015/04/29},
	abstract = {Mitochondria represent the major bioenergetic hub coordinating cellular and organismal homeostasis. The underlying causes of many pathologies tormenting humans converge on impaired mitochondrial maintenance. Mitochondria-specific autophagy (mitophagy), a cellular catabolic process targeting mitochondria, holds a prominent role in mitochondrial quality control. In addition to core autophagic machinery components, mitophagy exploits a variety of molecules that identify damaged or superfluous mitochondria and mediate their elimination. Signaling pathways integrating environmental and genetic stimuli interact with key mitophagy effectors to activate cellular stress response mechanisms, ultimately modulating health and lifespan. Here, we review the signaling cascades and molecular mechanisms that govern the process of mitophagy and discuss their involvement in ageing and neurodegeneration. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging.},
	keywords = {*Aging, Animals, Autophagy/*physiology, Energy homeostasis, Humans, Mitochondria/*physiology, mitophagy, Neurodegenerative Diseases, Neurodegenerative Diseases/*physiopathology, parkin, Pink1, Signal Transduction/physiology, stress response},
	isbn = {0006-3002 (Print)0006-3002 (Linking)},
	author = {Lionaki, E. and Markaki, M. and Palikaras, K. and Tavernarakis, N.}
}
