@article {26970,
	title = {Mitophagy in neurodegeneration and aging},
	journal = {Front Genet},
	volume = {3},
	year = {2012},
	note = {Palikaras, KonstantinosTavernarakis, NektariosengSwitzerlandFront Genet. 2012 Dec 19;3:297. doi: 10.3389/fgene.2012.00297. eCollection 2012.},
	pages = {297},
	edition = {2012/12/26},
	abstract = {Macroautophagy is a cellular catabolic process that involves the sequestration of cytoplasmic constituents into double-membrane vesicles known as autophagosomes, which subsequently fuse with lysosomes, where they deliver their cargo for degradation. The main physiological role of autophagy is to recycle intracellular components, under conditions of nutrient deprivation, so as to supply cells with vital materials and energy. Selective autophagy also takes place in nutrient-rich conditions to rid the cell of damaged organelles or protein aggregates that would otherwise compromise cell viability. Mitophagy is a selective type of autophagy, whereby damaged or superfluous mitochondria are eliminated to maintain proper mitochondrial numbers and quality control. While mitophagy shares key regulatory factors with the general macroautophagy pathway, it also involves distinct steps, specific for mitochondrial elimination. Recent findings indicate that parkin and the phosphatase and tensin homolog-induced putative kinase protein 1 (PINK1), which have been implicated in the pathogenesis of neurodegenerative diseases such as Parkinson{\textquoteright}s disease, also regulate mitophagy and function to maintain mitochondrial homeostasis. Here, we survey the molecular mechanisms that govern the process of mitophagy and discuss its involvement in the onset and progression of neurodegenerative diseases during aging.},
	keywords = {Aging, Autophagy, Mitochondria, mitophagy, Neurodegeneration, neuron, parkin, Pink1},
	isbn = {1664-8021 (Electronic)1664-8021 (Linking)},
	author = {Palikaras, K. and Tavernarakis, N.}
}
