Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28337125
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Mol+Neurosci
2017 ; 10
(ä): 64
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Neuronal Mitophagy in Neurodegenerative Diseases
#MMPMID28337125
Martinez-Vicente M
Front Mol Neurosci
2017[]; 10
(ä): 64
PMID28337125
show ga
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.