ArticleArthritis research & therapy2019
Romidepsin suppresses monosodium urate crystal-induced cytokine production through upregulation of suppressor of cytokine signaling 1 expression.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Gout Inflammation Time Programming: Molecular Clock from Crystal Triggering to Tissue Remodeling.International journal of molecular sciences · 2026Review
- RGFP966 inhibits activation of AIM2 inflammasomes to promote mitophagy to relieve acute gouty arthritis.PloS one · 2026Article
- Quercetin in metabolic diseases: mechanisms, therapeutics, and multidimensional frontiers.Frontiers in endocrinology · 2026Review
- Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.Frontiers in immunology · 2026Review
- DAMP-driven trained immunity: metabolic and epigenetic reprogramming in critical illness and chronic inflammation.Frontiers in immunology · 2025Review
- Epigenetic programming reshapes innate immune memory: decoding the molecular imprint of gouty inflammation.Frontiers in pharmacology · 2025Review
- Histone Deacetylase (HDAC) Inhibitors as a Novel Therapeutic Option Against Fibrotic and Inflammatory Diseases.Biomolecules · 2024Review
- Mechanism of flavonoids in the treatment of gouty arthritis (Review).Molecular medicine reports · 2024Review
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- A multidimensional platform of patient-derived tumors identifies drug susceptibilities for clinical lenvatinib resistance.Acta pharmaceutica Sinica. B · 2024Article
- Sirt3 improves monosodium urate crystal-induced inflammation by suppressing Acod1 expression.Arthritis research & therapy · 2023Article
- Histone Deacetylase 6 Inhibitor CKD-WID Suppressed Monosodium Urate-Induced Osteoclast Formation by Blocking Calcineurin-NFAT Pathway in RAW 264.7 Cells.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study.Signal transduction and targeted therapy · 2023Review
- An Epigenetic Insight into NLRP3 Inflammasome Activation in Inflammation-Related Processes.Biomedicines · 2021Review
- Autoinflammatory Features in Gouty Arthritis.Journal of clinical medicine · 2021Review
- Resveratrol Relieves Gouty Arthritis by Promoting Mitophagy to Inhibit Activation of NLRP3 Inflammasomes.Journal of inflammation research · 2021Article
- Immunomodulatory Effects of Histone Deacetylation Inhibitors in Graft-vs.-Host Disease After Allogeneic Stem Cell Transplantation.Frontiers in immunology · 2021Review
- T Helper Cell Lineage-Defining Transcription Factors: Potent Targets for Specific GVHD Therapy?Frontiers in immunology · 2021Review
- Where Epigenetics Meets Food Intake: Their Interaction in the Development/Severity of Gout and Therapeutic Perspectives.Frontiers in immunology · 2021Review
- LRRK2 Regulates CPT1A to Promote β-Oxidation in HepG2 Cells.Molecules (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundAcute gouty arthritis currently is the most common form of inflammatory arthritis in developed countries. Treatment is still suboptimal. Dosage of urate-lowering therapy is often too low to reach target urate levels, and adherence to therapy is poor. In this study, we therefore explore a new treatment option to limit inflammation in acute gout: specific histone deacetylase (HDAC) inhibition.
methodsPeripheral blood mononuclear cells (PBMCs) were cultured with a combination of monosodium urate crystals (MSU) and palmitic acid (C16.0) in order to activate the NLRP3 inflammasome and induce IL-1β production. HDAC inhibitors and other compounds were added beforehand with a 1-h pre-incubation period.
resultsThe HDAC1/2 inhibitor romidepsin was most potent in lowering C16.0+MSU-induced IL-1β production compared to other specific class I HDAC inhibitors. At 10 nM, romidepsin decreased IL-1β, IL-1Ra, IL-6, and IL-8 production. IL-1β mRNA was significantly decreased at 25 nM. Although romidepsin increased PTEN expression, PBMCs from patients with germline mutations in PTEN still responded well to romidepsin. Romidepsin also increased SOCS1 expression and blocked STAT1 and STAT3 activation. Furthermore, experiments with bortezomib showed that blocking the proteasome reverses the cytokine suppression by romidepsin.
conclusionsOur results show that romidepsin is a very potent inhibitor of C16.0+MSU-induced cytokines in vitro. Romidepsin upregulated transcription of SOCS1, which was shown to directly target inflammatory signaling molecules for proteasomal degradation. Inhibiting the proteasome therefore reversed the cytokine-suppressive effects of romidepsin. HDAC1/2 dual inhibition could therefore be a highly potent new treatment option for acute gout, although safety has to be determined in vivo.
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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.