Oxidative stress in the pathology and treatment of systemic lupus erythematosus

Perl, Andras

doi:10.1038/nrrheum.2013.147

Cited by 358Systemic Lupus Erythematosus ResearchAntioxidant Activity and Oxidative StressRedox biology and oxidative stress

Oxidative stress in the pathology and treatment of systemic lupus erythematosus

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Perl, Andras·2013·Nature Reviews Rheumatology

DOI 10.1038/nrrheum.2013.147PMC PMC4046645

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Abstract

Oxidative stress is increased in systemic lupus erythematosus (SLE), and it contributes to immune system dysregulation, abnormal activation and processing of cell-death signals, autoantibody production and fatal comorbidities. Mitochondrial dysfunction in T cells promotes the release of highly diffusible inflammatory lipid hydroperoxides, which spread oxidative stress to other intracellular organelles and through the bloodstream. Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE. In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine-protein kinase mTOR undergoes redox-dependent activation. In turn, reversal of glutathione depletion by application of its amino acid precursor, N-acetylcysteine, improves disease activity in lupus-prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research. Blocking mTOR activation in T cells could conceivably provide a well-tolerated and inexpensive alternative approach to B-cell blockade and traditional immunosuppressive treatments. Nevertheless, compartmentalized oxidative stress in self-reactive T cells, B cells and phagocytic cells might serve to limit autoimmunity and its inhibition could be detrimental. Antioxidant therapy might also be useful in ameliorating damage caused by other treatments. This Review thus seeks to critically evaluate the complexity of oxidative stress and its relevance to the pathogenesis and treatment of SLE.

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Metabolic aberrations induced by mitochondrial abnormalities are linked to self-reactive and inflammatory phenotypes in autoimmune conditions including SLE and rheumatoid arthritis.
“In various cell types, metabolic aberrations induced by mitochondrial abnormalities are linked to self-reactive and inflammatory phenotypes in autoimmune conditions, including SLE and RA68,69”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [68]
The sections on diminished antioxidant defences and oxidative autoantigenesis link mitochondrial dysfunction and oxidative stress in SLE to autoreactivity and inflammation. The section on increased mitochondrial ROI production also associates a mitochondrial-protein variant with predisposition to RA, but it does not establish the claimed link to self-reactive or inflammatory phenotypes in RA. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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These oxidative events can generate neoantigens that the adaptive immune system may recognize as exogenous threats.
“These events can lead to the generation of neoantigens that could be recognized as exogenous threats by the adaptive immune system68”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [68]

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Oxidative Stress in Systemic Lupus Erythematosus
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Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism
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Oxidative Stress – A Major Player in the Pathophysiology of Systemic Lupus Erythematosus
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Authors: Perl, A.
Venue: Nature Reviews Rheumatology
Publisher: Springer Science and Business Media LLC
Published: 2013-10-08
Volume: 9
Issue: 11
Pages: 674-686
ISSN: 1759-4790 (ISSN-L)
1759-4804
DOI: 10.1038/nrrheum.2013.147
PMC: PMC4046645
OpenAlex: W2078472057
Cited by: 358
References: 139
Citations by year: 2026: 18 · 2025: 44 · 2024: 36 · 2023: 18 · 2022: 28 · 2021: 32 · 2020: 36 · 2019: 27 · 2018: 25 · 2017: 19 · 2016: 33 · 2015: 28 · 2014: 14
FWCI: 3.98
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature Reviews Rheumatology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Allergy and Infectious Diseases (R01AI048079, R01AI072648, AI 048, AI 072)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (U01AR076092)
National Center for Complementary and Integrative Health (AT-004332, R01AT004332)
Topics: Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: oxidative stress, systemic lupus erythematosus, mitochondrial dysfunction, T cells, lipid hydroperoxides, glutathione depletion, mTOR, N-acetylcysteine, antioxidant therapy, autoimmunity, autoantibody production, disease activity, organ damage, lupus-prone mice
MeSH terms: Animals, Antioxidants, Humans, Lupus Erythematosus, Systemic, Autoimmunity, Oxidative Stress

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Oxidative stress in the pathology and treatment of systemic lupus erythematosus

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