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Oxidative stress in autoimmune rheumatic diseases
Miranda J Smallwood1, Ahuva Nissim2, Annie R Knight1
1University of Exeter Medical School, St Luke's Campus, Exeter, Devon EX1 2LU, UK.
Free Radical Biology & Medicine
|June 3, 2018
Summary
Oxidative stress from excess reactive oxygen and nitrogen species contributes to autoimmune diseases like rheumatoid arthritis. Targeting these species and enhancing antioxidant defenses shows promise for future therapies and diagnostics.
Area of Science:
- Immunology
- Biochemistry
- Rheumatology
Background:
- Autoimmune rheumatic diseases, such as rheumatoid arthritis, present management challenges.
- Oxidative stress, characterized by excess reactive oxygen species (ROS) and reactive nitrogen species (RNS), is implicated in autoimmune diseases.
- Sources of ROS/RNS include NADPH oxidases (NOXs), mitochondria, and specific enzymes.
Purpose of the Study:
- To explore the role of oxidative stress in autoimmune rheumatic diseases.
- To identify potential diagnostic biomarkers related to oxidative modifications.
- To discuss redox-based therapeutic strategies.
Main Methods:
- Review of literature on oxidative stress mechanisms in autoimmune diseases.
- Analysis of reactive species production and antioxidant systems.
- Identification of autoantibodies as potential diagnostic markers.
Main Results:
- Oxidative stress arises when ROS/RNS production overwhelms antioxidant capacity.
- Oxidative protein modifications can create neoepitopes, triggering autoantibody formation.
- Anti-carbamylated protein and anti-oxidized type II collagen antibodies show diagnostic potential.
Conclusions:
- Understanding oxidative stress pathways is crucial for managing autoimmune diseases.
- Autoantibodies against specific oxidized antigens offer promising diagnostic and monitoring tools.
- Future therapies may involve modulating cellular antioxidant systems or targeting ROS/RNS sources.
Keywords:
3-nitrotyrosineAntioxidant enzymeAutoimmunityClinical markerHydrogen peroxideHydrogen sulfideNADPH oxidaseNitric oxide synthaseNitrite reductasePeroxiredoxinPost-translational modificationReactive nitrogen speciesReactive oxygen speciesReactive sulfur speciesRheumatoid arthritisSclerodermaSjögren's syndromeSuperoxide anion radicalSystemic lupus erythematosusThioredoxin
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