ArticleArthritis research & therapy2023
Deubiquitinase USP16 induces gouty arthritis via Drp1-dependent mitochondrial fission and NLRP3 inflammasome activation.
Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- Mitochondria as convergence hubs for innate immunity pathways.Communications biology · 2026Review
- USP16 regulates mitochondrial function by deubiquitinating TOM40, a core component of the translocase in the mitochondrial outer membrane.Cell death & disease · 2026Article
- Diacerein ameliorates acute urarthritis in rats through the Nrf-2/HO-1 and NF-κB pathways.Inflammopharmacology · 2026Article
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- USP16 S-nitrosylation aggravates coronary microembolization-induced myocardial injury via repressing KDM1A-mediated glutathione homeostasis.Nature communications · 2025Article
- Polycomb Repressive Complex 1 and USP16 localize to the mitochondrion and influence its function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- Exploring the correlation between Drp1 protein and the neurotoxicity of propofol.Frontiers in neuroscience · 2025Review
- The Progress of Immune Cells-induced Inflammatory Response in Gout.Current pharmaceutical design · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Epigenetic programming reshapes innate immune memory: decoding the molecular imprint of gouty inflammation.Frontiers in pharmacology · 2025Review
- Multiomics Identifies Potential Biomarkers in Ankylosing Spondylitis Bone Formation.Human mutation · 2025Article
- The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.Biomolecules & biomedicine · 2024Review
- Targeting Neutrophil Extracellular Traps in Gouty Arthritis: Insights into Pathogenesis and Therapeutic Potential.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGouty arthritis is the most frequently diagnosed inflammatory arthritis worldwide. Dynamin-related protein 1 (Drp1), a regulator of mitochondrial fission, contributes to various inflammatory disorders via activating NLRP3 inflammasome. However, the biological role of Drp1 in gouty arthritis remains undefined.
methodsA mouse model of monosodium urate (MSU)-induced gouty arthritis and MSU-stimulated macrophages were established as in vivo and in vitro models, respectively. Histological changes were assessed by H&E and IHC analysis. RT-qPCR and western blot were used to detect the expression of Drp1 and the key molecules in joint tissues and macrophages. Cytokine secretion was measured by ELISA assay, and antioxidant enzymes activities and LDH release were monitored using commercial kits. Mitochondrial structure and functions were assessed by transmission electron microscopy (TEM) and MitoSOX staining. Co-IP and GST pull-down assay were used to detect the direct interaction between USP16 and Drp1, as well as the ubiquitination of Drp1.
resultsDrp1 was elevated in MSU-induced gouty arthritis model, and it induced gouty arthritis via NF-κB pathway and NLRP3 inflammasome activation. In addition, Drp1 activated NF-κB/NLRP3 signaling via modulating mitochondrial fission. Mechanistically, USP16 mediated deubiquitination and stabilization of Drp1 through its direct interaction with Drp1. Functional studies further showed that USP16 was highly expressed in MSU-stimulated macrophages and induced gouty arthritis via Drp1-dependent NLRP3 inflammasome activation.
conclusionDeubiquitinase USP16 induced gouty arthritis via Drp1-dependent mitochondrial fission and NF-κB/NLRP3 signaling.
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