ReviewFrontiers in immunology2026
Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Microbiota-Derived Metabolites in the Epigenetic Regulation of Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arthritis comprises a spectrum of immune-mediated joint disorders, with rheumatoid arthritis (RA) representing prototypic autoimmunity and psoriatic arthritis (PsA) and ankylosing spondylitis (AS) spanning an autoinflammation-autoimmunity continuum. Across this spectrum, oxidative stress and inflammatory signaling reinforce each other within synovial/entheseal niches, sustaining immune activation and progressive structural damage. Excess reactive oxygen species (ROS) injure chondrocytes and synoviocytes, activate NF-κB and the NLRP3 inflammasome, and reprogram stromal-immune interactions; inflammatory mediators further increase ROS via NADPH oxidases, mitochondrial dysfunction, and immunometabolic perturbations, sustaining a "ROS-inflammation-ROS" loop. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-responsive transcription factor that, upon release from Keap1, drives antioxidant response element-dependent cytoprotective programs. Beyond antioxidation, Nrf2 can dampen NF-κB-linked transcription and modulate ferroptosis, pyroptosis, and autophagy while shaping macrophage and fibroblast-like synoviocyte states. Collectively, these actions position Nrf2 as a context-dependent redox checkpoint that may constrain inflammatory amplification and tune autoimmune-relevant processes (e.g., inflammatory antigen presentation and effector persistence) largely via microenvironmental remodeling rather than direct TCR/BCR inhibition. Here, we (i) map Nrf2-dependent versus Nrf2-independent nodes in the oxidative stress-inflammation circuit; (ii) compare cell type- and subtype-specific Nrf2 functions across RA, PsA, and AS; (iii) summarize pharmacologic and natural-product Nrf2 activators together with joint-targeted delivery strategies; and (iv) discuss evidence and gaps for Nrf2 in core autoimmune mechanisms, including self-tolerance, antigen handling, and pathogenic immune memory. This synthesis highlights Nrf2 as a mechanistic bridge between redox balance and immune regulation, informing Nrf2-centered therapies for autoimmune and immune-mediated arthritides.
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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 Socratic graph.