Role of Methionine Oxidation in the Progression of Oxidative Stress and Age-Related Diseases
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Aberrant Oxidation of Biomolecules".
Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 1769
Special Issue Editor
Special Issue Information
Dear Colleagues,
Oxidative stress in biological systems may lead to the oxidation of methionine of both proteins and of the free amino acid methionine. The resulting methionine sulfoxide (MetO) moiety exists in two enantiomer forms: S-MetO and R-MetO, which can be enzymatically reduced to methionine through the methionine sulfoxide reductase (Msr) system (comparising of MsrA and MsrB, respectively). Oxidation of methionine residues of proteins may cause changes in the structure and function of the targeted proteins. In turn, these changes may foster the development of cellular and extracellular abnormalities that are associated with age-related diseases. The ability of an organism to reduce or degrade the MetO-containg proteins contributes to its cellular antioxidant capacity that may also affect its survival. Thus, the interaction between the Msr and the protein degradation systems, together with oxidative-stress-related signaling, play an important role in determining the redox and disease state of a cell/organism. The current Special Issue aims to gather both original and review articles that describe recent advances in scientific knowledge linked to methionine oxidation, such as function of age and conditions of oxidative stress. It is hoped that a better understanding of the physiological involvement of methionine oxidation and reduction in a living cell will foster the development of novel treatments to age and oxidative-stress-associated diseases.
Dr. Jackob Moskovitz
Guest Editor
Manuscript Submission Information
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Keywords
- oxidative stress
- methionine oxidation
- aging
- post-translation modification
- methionine sulfoxide
- methionine sulfoxide reductase
