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Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

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Date
2018
Author(s)
Hyttinen, Juha MT
Viiri, Johanna
Kaarniranta, Kai
Blasiak, Janusz
Unique identifier
10.1007/s00018-018-2843-7
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Self-archived article

Citation
Hyttinen, Juha MT. Viiri, Johanna. Kaarniranta, Kai. Blasiak, Janusz. (2018). Mitochondrial quality control in AMD: does mitophagy play a pivotal role?.  CELLULAR AND MOLECULAR LIFE SCIENCES: CMLS, [First Online: 18 May 2018], 10.1007/s00018-018-2843-7.
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© Springer International Publishing AG, part of Springer Nature
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All rights reserved. This is a post-peer-review, pre-copyedit version of an article published in CELLULAR AND MOLECULAR LIFE SCIENCES: CMLS. The final authenticated version is available online at: http://dx.doi.org/10.1007/s00018-018-2843-7
Abstract

Age-related macular degeneration (AMD) is the predominant cause of visual loss in old people in the developed world, whose incidence is increasing. This disease is caused by the decrease in macular function, due to the degeneration of retinal pigment epithelium (RPE) cells. The aged retina is characterised by increased levels of reactive oxygen species (ROS), impaired autophagy, and DNA damage that are linked to AMD pathogenesis. Mitophagy, a mitochondria-specific type of autophagy, is an essential part of mitochondrial quality control, the collective mechanism responsible for this organelle’s homeostasis. The abundance of ROS, DNA damage, and the excessive energy consumption in the ageing retina all contribute to the degeneration of RPE cells and their mitochondria. We discuss the role of mitophagy in the cell and argue that its impairment may play a role in AMD pathogenesis. Thus, mitophagy as a potential therapeutic target in AMD and other degenerative diseases is as well explored.

Subjects
cell senescence   mitochondrial DNA damage   Nrf2/PGC-1α axis   oxidative damage   ubiquitin   
URI
https://erepo.uef.fi/handle/123456789/6668
Link to the original item
http://dx.doi.org/10.1007/s00018-018-2843-7
Publisher
Springer Nature
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  • Terveystieteiden tiedekunta [1324]
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