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Neuronal Mitophagy in Neurodegenerative Diseases
Martinez-Vicente, Marta (Hospital Universitari Vall d'Hebron. Institut de Recerca)

Fecha: 2017
Resumen: Neuronal homeostasis depends on the proper functioning of different quality control systems. All intracellular components are subjected to continuous turnover through the coordinated synthesis, degradation and recycling of their constituent elements. Autophagy is the catabolic mechanism by which intracellular cytosolic components, including proteins, organelles, aggregates and any other intracellular materials, are delivered to lysosomes for degradation. Among the different types of selective autophagy described to date, the process of mitophagy involves the selective autophagic degradation of mitochondria. In this way, mitophagy is responsible for basal mitochondrial turnover, but can also be induced under certain physiological or pathogenic conditions to eliminate unwanted or damaged mitochondria. Dysfunctional cellular proteolytic systems have been linked extensively to neurodegenerative diseases (ND) like Alzheimer's disease (AD), Parkinson's disease (PD), or Huntington's disease (HD), with autophagic failure being one of the main factors contributing to neuronal cell death in these diseases. Neurons are particularly vulnerable to autophagic impairment as well as to mitochondrial dysfunction, due mostly to their particular high energy dependence and to their post-mitotic nature. The accurate and proper degradation of dysfunctional mitochondria by mitophagy is essential for maintaining control over mitochondrial quality and quantity in neurons. In this report, I will review the role of mitophagy in neuronal homeostasis and the consequences of its dysfunction in ND.
Nota: Número d'acord de subvenció ISCIII/CP09-00184
Nota: Número d'acord de subvenció ISCIII/PI14-01529
Nota: Número d'acord de subvenció ISCIII/MSII15-00007
Nota: Número d'acord de subvenció MINECO/SAF2009-08374
Derechos: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original. Creative Commons
Lengua: Anglès
Documento: article ; article de revisió ; publishedVersion
Materia: Mitophagy ; Autophagy ; Neurodegeneration ; Parkinson's disease ; Alzheimer disease
Publicado en: Frontiers in molecular neuroscience, Vol. 10 (march 2017) , ISSN 1662-5099

DOI: 10.3389/fnmol.2017.00064
PMID: 28337125


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