Abstract
Proteins are constantly exposed to environmental stressors such as free radicals and heat shock leading to their misfolding and later to aggregation. In particular mitochondrial proteins are challenged by reactive oxygen species (ROS) due to the oxidative metabolism of the organelle. Protein aggregation has been associated with a wide variety of pathological conditions called proteopathies. However, for the maintenance of protein and cellular homeostasis, mitochondria have developed an elaborate protein quality control system consisting of chaperones and ATP-dependent proteases, specifically employed to rescue this organelle from damage due to the accumulation of misfolded proteins and toxic aggregates. Aging is characterized by a general decline of mitochondrial functions, correlating with a decrease in mitochondrial protein quality control activity and an increase of free radical production. In particular in age-related diseases like neurodegeneration, a correlation between mitochondrial damage and disease onset has been established. In this review we summarize the current knowledge about mitochondrial protein quality control mechanisms in mammalian cells, with a special emphasis on the role in oxidative stress and in neurodegenerative diseases.
Keywords: Alzheimer disease, mitochondrial protein quality control (mtPQC), oxidative stress, Parkinson disease.
Current Alzheimer Research
Title:Role of Mitochondrial Protein Quality Control in Oxidative Stress-induced Neurodegenerative Diseases
Volume: 13 Issue: 2
Author(s): Giovanna Cenini and Wolfgang Voos
Affiliation:
Keywords: Alzheimer disease, mitochondrial protein quality control (mtPQC), oxidative stress, Parkinson disease.
Abstract: Proteins are constantly exposed to environmental stressors such as free radicals and heat shock leading to their misfolding and later to aggregation. In particular mitochondrial proteins are challenged by reactive oxygen species (ROS) due to the oxidative metabolism of the organelle. Protein aggregation has been associated with a wide variety of pathological conditions called proteopathies. However, for the maintenance of protein and cellular homeostasis, mitochondria have developed an elaborate protein quality control system consisting of chaperones and ATP-dependent proteases, specifically employed to rescue this organelle from damage due to the accumulation of misfolded proteins and toxic aggregates. Aging is characterized by a general decline of mitochondrial functions, correlating with a decrease in mitochondrial protein quality control activity and an increase of free radical production. In particular in age-related diseases like neurodegeneration, a correlation between mitochondrial damage and disease onset has been established. In this review we summarize the current knowledge about mitochondrial protein quality control mechanisms in mammalian cells, with a special emphasis on the role in oxidative stress and in neurodegenerative diseases.
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Cite this article as:
Cenini Giovanna and Voos Wolfgang, Role of Mitochondrial Protein Quality Control in Oxidative Stress-induced Neurodegenerative Diseases, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205012666150921103213
DOI https://dx.doi.org/10.2174/1567205012666150921103213 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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