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Mitochondrial and Ubiquitin Proteasome System Dysfunction in Ageing and Disease: Two Sides of the Same Coin?

Department of Neuroscience, Karolinska Institutet, Retzius väg 8, Stockholm 171 77, Sweden
Authors to whom correspondence should be addressed.
Academic Editor: Irmgard Tegeder
Int. J. Mol. Sci. 2015, 16(8), 19458-19476;
Received: 9 May 2015 / Revised: 23 July 2015 / Accepted: 7 August 2015 / Published: 17 August 2015
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases)
Mitochondrial dysfunction and impairment of the ubiquitin proteasome system have been described as two hallmarks of the ageing process. Additionally, both systems have been implicated in the etiopathogenesis of many age-related diseases, particularly neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease. Interestingly, these two systems are closely interconnected, with the ubiquitin proteasome system maintaining mitochondrial homeostasis by regulating organelle dynamics, the proteome, and mitophagy, and mitochondrial dysfunction impairing cellular protein homeostasis by oxidative damage. Here, we review the current literature and argue that the interplay of the two systems should be considered in order to better understand the cellular dysfunction observed in ageing and age-related diseases. Such an approach may provide valuable insights into molecular mechanisms underlying the ageing process, and further discovery of treatments to counteract ageing and its associated diseases. Furthermore, we provide a hypothetical model for the heterogeneity described among individuals during ageing. View Full-Text
Keywords: ageing; mitochondria; ubiquitin; proteasome; ROS ageing; mitochondria; ubiquitin; proteasome; ROS
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Ross, J.M.; Olson, L.; Coppotelli, G. Mitochondrial and Ubiquitin Proteasome System Dysfunction in Ageing and Disease: Two Sides of the Same Coin? Int. J. Mol. Sci. 2015, 16, 19458-19476.

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