Proteostasis, oxidative stress and aging

The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functiona...

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Published inRedox biology Vol. 13; no. C; pp. 550 - 567
Main Authors Korovila, Ioanna, Hugo, Martín, Castro, José Pedro, Weber, Daniela, Höhn, Annika, Grune, Tilman, Jung, Tobias
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.10.2017
Elsevier
Subjects
Online AccessGet full text
ISSN2213-2317
2213-2317
DOI10.1016/j.redox.2017.07.008

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Abstract The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells. [Display omitted]
AbstractList The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed "proteostasis". Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the "ubiquitin-proteasomal system" (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the "autophagy-lysosomal system", which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells.
The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed "proteostasis". Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the "ubiquitin-proteasomal system" (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the "autophagy-lysosomal system", which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells.The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed "proteostasis". Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the "ubiquitin-proteasomal system" (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the "autophagy-lysosomal system", which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells.
The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells. fx1
The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates. Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells. [Display omitted]
Author Korovila, Ioanna
Hugo, Martín
Höhn, Annika
Weber, Daniela
Grune, Tilman
Castro, José Pedro
Jung, Tobias
AuthorAffiliation b German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany
d NutriAct – Competence Cluster Nutrition Research Berlin-Potsdam, 14558 Nuthetal, Germany
a Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
f Institute for Innovation and Health Research (I3S), Aging and Stress Group, R. Alfredo Allen, 4200-135 Porto, Portugal
c German Center for Cardiovascular Research (DZHK), 10117 Berlin, Germany
e Faculty of Medicine, Department of Biomedicine, University of Porto, 4200-319, Portugal
AuthorAffiliation_xml – name: e Faculty of Medicine, Department of Biomedicine, University of Porto, 4200-319, Portugal
– name: f Institute for Innovation and Health Research (I3S), Aging and Stress Group, R. Alfredo Allen, 4200-135 Porto, Portugal
– name: d NutriAct – Competence Cluster Nutrition Research Berlin-Potsdam, 14558 Nuthetal, Germany
– name: a Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– name: b German Center for Diabetes Research (DZD), 85764 Muenchen-Neuherberg, Germany
– name: c German Center for Cardiovascular Research (DZHK), 10117 Berlin, Germany
Author_xml – sequence: 1
  givenname: Ioanna
  surname: Korovila
  fullname: Korovila, Ioanna
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 2
  givenname: Martín
  surname: Hugo
  fullname: Hugo, Martín
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 3
  givenname: José Pedro
  surname: Castro
  fullname: Castro, José Pedro
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 4
  givenname: Daniela
  surname: Weber
  fullname: Weber, Daniela
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 5
  givenname: Annika
  surname: Höhn
  fullname: Höhn, Annika
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 6
  givenname: Tilman
  surname: Grune
  fullname: Grune, Tilman
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
– sequence: 7
  givenname: Tobias
  surname: Jung
  fullname: Jung, Tobias
  email: tobias.jung@dife.de
  organization: Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28763764$$D View this record in MEDLINE/PubMed
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Keywords Redox shift
Oxidative stress
Autophagy
Lysosome
Proteasome
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Snippet The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular...
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SubjectTerms Aging - metabolism
Animals
Autophagy
Glycation End Products, Advanced - metabolism
Humans
Lipofuscin - metabolism
Lysosome
Oxidative Stress
Proteasome
Proteostasis
Redox shift
Review
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Title Proteostasis, oxidative stress and aging
URI https://dx.doi.org/10.1016/j.redox.2017.07.008
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