ReviewFrontiers in cell and developmental biology2026
The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed.
- Combined in vitro microcurrent stimulation and celecoxib suppress NF-κB/NLRP3 signaling and cartilage catabolism in human chondrocytes.Immunologic research · 2026Article
- Redox-Regulating Propolis- and Honey-Containing Hydrogels in Osteoarthritis.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Stress in Animals: A Systematic Analysis from Signaling Pathways to Biological Effects.Life (Basel, Switzerland) · 2026Review
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- REJENERAInflammopharmacology · 2026Article
- Neoagarohexaose Attenuates Inflammatory and Oxidative Joint Injury in MIA/CIOA Mouse Models of Osteoarthritis.International journal of molecular sciences · 2026Article
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arthritis, a group of common diseases characterized by joint inflammation, cartilage destruction, and imbalance in bone remodeling, has high global prevalence and disability rates. In recent years, oxidative stress and chronic inflammation have been widely recognized as core mechanisms jointly driving its pathological process. The antioxidant response axis formed by nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) plays a key role in maintaining joint tissue redox balance and suppressing excessive inflammatory responses. Extensive basic and translational research indicates that the Nrf2/HO-1 pathway exerts protective effects through multiple mechanisms: reducing reactive oxygen species (ROS) levels, inhibiting nuclear factor-kappa B (NF-κB)-mediated inflammation, regulating macrophage polarization, and influencing processes such as apoptosis, ferroptosis, and fibrosis, thereby significantly alleviating tissue damage and clinical symptoms in arthritis. Currently, various natural products, small-molecule compounds, and drug repurposing strategies targeting the activation or regulation of this pathway have shown promising joint protective effects in animal experiments, suggesting Nrf2/HO-1 is a potential disease-modifying therapeutic target. This review systematically summarizes the latest research progress on the role of Nrf2/HO-1 in the pathogenesis of arthritis, experimental evidence from cellular and animal models, therapeutic strategies targeting this pathway, and discusses key scientific and technical challenges for future clinical translation.
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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 OpenQuestion graph.