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Mitochondria, autophagy and age-associated neurodegenerative diseases: New insights into a complex interplay.

Authors
Type
Published Article
Journal
Biochimica et Biophysica Acta
0006-3002
Publisher
Elsevier
Publication Date
Volume
1847
Issue
11
Pages
1412–1423
Identifiers
DOI: 10.1016/j.bbabio.2015.04.010
PMID: 25917894
Source
Medline
Keywords
License
Unknown

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.

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