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1000 Titel
  • Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence
1000 Autor/in
  1. Höhn, Annika |
  2. Weber, Daniela |
  3. Jung, Tobias |
  4. Ott, Christiane |
  5. Hugo, Martín |
  6. Kochlik, Bastian |
  7. Kehm, Richard |
  8. König, Jeanette |
  9. Grune, Tilman |
  10. Castro, José Pedro |
1000 Erscheinungsjahr 2016
1000 LeibnizOpen
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2016-12-07
1000 Erschienen in
1000 Quellenangabe
  • 11: 482-501
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2016
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1016/j.redox.2016.12.001 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228102/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies) by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.
1000 Sacherschließung
lokal Micronutrients
lokal Aging
lokal Senescence
lokal Trace elements
lokal Proteostasis
lokal Protein oxidation
lokal Antioxidants
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://orcid.org/0000-0003-1306-2668|https://orcid.org/0000-0002-2054-6233|https://frl.publisso.de/adhoc/creator/SnVuZywgVG9iaWFz|https://frl.publisso.de/adhoc/creator/T3R0LCBDaHJpc3RpYW5l|http://orcid.org/0000-0003-3430-6457|https://frl.publisso.de/adhoc/creator/S29jaGxpaywgQmFzdGlhbg==|https://frl.publisso.de/adhoc/creator/S2VobSwgUmljaGFyZA==|https://frl.publisso.de/adhoc/creator/S8O2bmlnLCBKZWFuZXR0ZQ==|http://orcid.org/0000-0003-4775-9973|https://frl.publisso.de/adhoc/creator/Q2FzdHJvLCBKb3PDqSBQZWRybw==
1000 Label
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1000 Förderprogramm
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1000 Dateien
1000 Objektart article
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1000 @id frl:6406124.rdf
1000 Erstellt am 2018-01-04T12:50:40.766+0100
1000 Erstellt von 122
1000 beschreibt frl:6406124
1000 Bearbeitet von 122
1000 Zuletzt bearbeitet 2021-04-21T10:42:24.834+0200
1000 Objekt bearb. Wed Apr 21 10:42:24 CEST 2021
1000 Vgl. frl:6406124
1000 Oai Id
  1. oai:frl.publisso.de:frl:6406124 |
1000 Sichtbarkeit Metadaten public
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