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Int J Biochem Cell Biol. 2016 Oct;79:382-387. doi: 10.1016/j.biocel.2016.08.019. Epub 2016 Aug 30.

Mitophagy and the therapeutic clearance of damaged mitochondria for neuroprotection.

Author information

1
Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, United Kingdom; Regina Elena-National Cancer Institute, 00144 Rome, Italy.
2
Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, United Kingdom; University College London Consortium for Mitochondrial Research, Royal College Street, NW1 0TU London, United Kingdom; Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy; Regina Elena-National Cancer Institute, 00144 Rome, Italy. Electronic address: mcampanella@rvc.ac.uk.

Abstract

Mitochondria are the foremost producers of the cellular energy currency ATP. They are also a significant source of reactive oxygen species and an important buffer of intracellular calcium. Mitochondrial retrograde signals regulate energy homeostasis and pro-survival elements whereas anterograde stimuli can trigger programmed cell death. Maintenance of a healthy, functional mitochondria network is therefore essential, and several mechanisms of mitochondrial quality control have been described. Mitochondrial dysfunction is linked to several neurodegenerative conditions including Parkinson, and Huntingdon diseases as well as Amyotrophic lateral sclerosis. Understanding the mechanisms governing mitochondrial quality control may reveal novel strategies for pharmacological intervention and disease therapy.

KEYWORDS:

Mitochondria; Mitophagy; Neurodegeneration; Therapy

PMID:
27586258
DOI:
10.1016/j.biocel.2016.08.019
[Indexed for MEDLINE]

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