ArticleLupus science & medicine2020
Targeting mitochondrial oxidative stress with MitoQ reduces NET formation and kidney disease in lupus-prone MRL-
Article in Lupus science & medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Diverse Roles of NETosis in the Pathogenesis of Lupus.Frontiers in immunology · 2022Pooled it
- Eight weeks of MitoQ supplementation does not alter kidney function or urinary kidney injury biomarkers in middle-aged and older adults.American journal of physiology. Renal physiology · 2026Trial
- Acute high-dose MitoQ does not increase urinary kidney injury markers in healthy adults: a randomized crossover trial.American journal of physiology. Renal physiology · 2024Trial
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- FAS-controlled T cells drive lymphoproliferation through glycolysis without effector differentiation.Journal of human immunity · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- Mesenchymal stem cell transplantation alleviated TBI-induced lung injury by inhibiting PAD4-dependent NET formation.Journal of advanced research · 2026Article
- A comprehensive insight into NETosis-extracellular vesicle crosstalk in autoimmune diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Role of Antioxidants in Diseases and its Impact on Mitochondria with A Focus on Diabetes: An Overview.Current drug research reviews · 2026Review
- Iron metabolism and ferroptosis: druggable targets to delay the progression of lupus nephritis.American journal of physiology. Renal physiology · 2026Review
- Neutrophil Extracellular Traps in Systemic Lupus Erythematosus: Pathogenic Mechanisms, Crosstalk with Oxidative Stress, and Antioxidant Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Challenges and strategies in clinical applications of CAR-T therapy for autoimmune diseases.Journal of hematology & oncology · 2025Review
- Mitochondrial dysfunction in myeloid cells: a central deficit in autoimmune diseases.Trends in immunology · 2025Review
- Succinate Dehydrogenase Subunit A (SDHA) Mediated Microglia Extracellular Traps Formation Participating in Cerebral Ischemic Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advances in Longevity: The Intersection of Regenerative Medicine and Cosmetic Dermatology.Journal of cosmetic dermatology · 2025Review
- Immunometabolism in systemic lupus erythematosus.Nature reviews. Rheumatology · 2025Review
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- From powerhouse to modulator: regulating immune system responses through intracellular mitochondrial transfer.Cell communication and signaling : CCS · 2025Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
objectivesRecent investigations in humans and mouse models with lupus have revealed evidence of mitochondrial dysfunction and production of mitochondrial reactive oxygen species (mROS) in T cells and neutrophils. This can provoke numerous cellular changes including oxidation of nucleic acids, proteins, lipids and even induction of cell death. We have previously observed that in T cells from patients with lupus, the increased mROS is capable of provoking oligomerisation of mitochondrial antiviral stimulator (MAVS) and production of type I interferon (IFN-I). mROS in SLE neutrophils also promotes the formation of neutrophil extracellular traps (NETs), which are increased in lupus and implicated in renal damage. As a result, in addition to traditional immunosuppression, more comprehensive treatments for lupus may also include non-immune therapy, such as antioxidants.
methodsLupus-prone MRL-
resultsMitoQ-treated mice manifested reduced neutrophil ROS and NET formation, decreased MAVS oligomerisation and serum IFN-I, and reduced immune complex formation in kidneys, despite no change in serum autoantibody .
conclusionsThese findings reveal the potential utility of targeting mROS in addition to traditional immunosuppressive therapy for lupus.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.