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Protein oxidation in aging: endoplasmic reticulum as a target
D van der Vlies1, J Woudenberg, J A Post
1Erasmus MC, Department of Internal Oncology - Josephina Nefkens Instituut, Rotterdam, The Netherlands. d.vandervlies@erasmucmc.nl
Amino Acids
|December 9, 2003
Summary
Protein oxidation increases with age, varying by tissue and species. The endoplasmic reticulum (ER) may play a role in aging due to oxidative damage and impaired function.
Area of Science:
- Biogerontology
- Molecular Biology
- Cellular Aging
Background:
- Oxidatively modified proteins accumulate with organismal and tissue age.
- Susceptibility to protein oxidation is influenced by tissue type, age, and species' maximum lifespan potential.
- Declining antioxidant defenses and protein localization impact oxidative damage levels during aging.
Purpose of the Study:
- To review the evidence linking endoplasmic reticulum (ER) dysfunction and oxidative stress to the aging process.
- To explore the role of the oxidized ER in cellular aging and age-related decline.
Main Methods:
- Literature review focusing on studies investigating protein oxidation, ER stress, and aging.
- Analysis of experimental data correlating protein oxidation levels with age and lifespan.
- Examination of molecular markers associated with ER stress and calcium homeostasis.
Main Results:
- Oxidative protein modification correlates with aging across species and tissues.
- Endoplasmic reticulum (ER) resident proteins are preferentially oxidized.
- Upregulation of ER stress chaperones and disturbed calcium homeostasis suggest ER involvement in aging.
Conclusions:
- Oxidative damage to the endoplasmic reticulum (ER) is a potential contributor to the aging process.
- ER dysfunction, characterized by oxidative stress and impaired calcium regulation, may drive age-related cellular decline.
- Targeting ER stress and oxidative pathways could offer insights into mitigating aging.
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