UPS Activation in the Battle Against Aging and Aggregation-Related Diseases: An Extended Review

Papaevgeniou, Nikoletta; Chondrogianni, Niki

doi:10.1007/978-1-4939-3756-1_1

Cited by 19 publications

(12 citation statements)

References 444 publications

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“…In the ATP-dependent degradation, the protein to be degraded is recognized by the proteasome through tagging with a small, evolutionarily conserved protein, namely ubiquitin; at least four molecules of ubiquitin serve as a signal for proteasomal degradation. This conjugation occurs through the tightly coordinated action of three different enzymes, namely E1, E2 and E3 [ 98 ]. Peptides and partially unfolded proteins, including oxidized proteins, were reported to be degraded in an ATP- and ubiquitin-independent manner [ 99 ].…”

Section: Molecular and Cellular Effects Of Oxidative Stress In Polyq Diseasesmentioning

confidence: 99%

“…Whether proteasome activation assists in the clearance of oxidized proteins that accumulate in HD or it degrades mutant Htt before it gets highly aggregated, or both is not completely clear yet. Regardless of its exact role, the proteasome comprises a promising therapeutic target against HD as it is for many other aggregation-related NDDs [ 98 ].…”

Section: Molecular and Cellular Effects Of Oxidative Stress In Polyq Diseasesmentioning

confidence: 99%

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Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

et al. 2021

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Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which are associated with selective neuronal degeneration. Several lines of evidence indicate that these mutant proteins are associated with oxidative stress, proteasome impairment and microglia activation. These events may correlate with the induction of inflammation in the nervous system and disease progression. Here, we review the effect of polyQ-induced oxidative stress in cellular and animal models of polyQ diseases. Furthermore, we discuss the interplay between oxidative stress, neurodegeneration and neuroinflammation using as an example the well-known neuroinflammatory disease, Multiple Sclerosis. Finally, we review some of the pharmaceutical interventions which may delay the onset and progression of polyQ disorders by targeting disease-associated mechanisms.

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Section: Molecular and Cellular Effects Of Oxidative Stress In Polyq Diseasesmentioning

confidence: 99%

Section: Molecular and Cellular Effects Of Oxidative Stress In Polyq Diseasesmentioning

confidence: 99%

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

et al. 2021

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“…Under specific conditions (such as aging, age-related conditions and diseases), the activity of the proteasome has been shown to be compromised. Several studies have focused on the activation of the proteasome (either in cellular models or in model organisms) to alleviate the negative effects of the above-mentioned processes [37], [38], [39], [40], [41], [42], [43], [44]. The proteasome activity has been shown to be increased through the induced expression of several subunits (core and/or regulatory ones) that ultimately lead to enhanced proteasome assembly and/or function.…”

Section: Proteasome Systemmentioning

confidence: 99%

Redox regulation of proteasome function

2017

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Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) were initially regarded mainly as metabolic by-products with damaging properties. Over the last decade, our understanding of their role in metabolism was drastically changed and they were recognized as essential mediators in cellular signaling cascades, as well as modulators of biochemical pathways. Proteostasis is highly affected by the various levels of intracellular and extracellular free radicals with either mild or severe outcomes. As part of the proteostatic network, the proteasome system is equally affected by redox alterations. This short review summarizes the effects of oxidative stress on proteasome status while it also recapitulates conditions and processes where redox alterations signal changes to proteasome expression, assembly and function.

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“…Proteostatic mechanisms and especially the proteasome, are highly affected by ageing [4] while loss of proteostasis features among the hallmarks of ageing [1]. Activation of the proteasome either through genetic means or through natural compounds has been suggested as a promising anti-ageing strategy [5].…”

Section: Anti-ageing Compoundsmentioning

confidence: 99%

Quest for Bioactive Compounds in Our Diet with Anti-Ageing and Anti-Aggregation Properties

Papaevgeniou

Panagiotidou

Filippopoulou

et al. 2019

CA16112 - Luxemburg 2019

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Ageing is a complex process affected by both genetic and environmental factors, characterized by a gradual failure of functionality, reduced stress response and resistance, leading to enhanced probability for age-related diseases and mortality. During the last decades, natural compounds have attracted the attention of researchers in the quest of bioactive phytochemicals with anti-ageing properties. For a few of these compounds an extra advantage appears; many of them have been shown to decelerate the progression of age-related diseases with emphasis on aggregation-related diseases. Using the nematode Caenorhabditis elegans along with the replicative senescence model of human primary fibroblasts, we have identified compounds that are part of our diet with anti-oxidation, anti-ageing and anti-aggregation activities. Some of the identified compounds promote their anti-ageing activity through activation of the proteasome, others through the activation of Nrf2 transcription factor, while others through inhibition of glucose transporters (GLUTs). Our work identifies new bioactive compounds with anti-ageing and/or anti-aggregation properties or reveals additional beneficial properties on already known bioactive compounds.

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UPS Activation in the Battle Against Aging and Aggregation-Related Diseases: An Extended Review

Cited by 19 publications

References 444 publications

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

Redox regulation of proteasome function

Quest for Bioactive Compounds in Our Diet with Anti-Ageing and Anti-Aggregation Properties

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