ArticleInflammation2013
Therapeutic effects of NK-HDAC-1, a novel histone deacetylase inhibitor, on collagen-induced arthritis through the induction of apoptosis of fibroblast-like synoviocytes.
Article in Inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- The epigenetic landscape of rheumatoid arthritis: Pathogenesis and drug therapeutic potentials.Acta pharmaceutica Sinica. B · 2025Review
- Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.Cell biochemistry and biophysics · 2025Review
- Epi-revolution in rheumatology: the potential of histone deacetylase inhibitors for targeted rheumatoid arthritis intervention.Inflammopharmacology · 2024Review
- Unveiling Novel Drug Targets and Emerging Therapies for Rheumatoid Arthritis: A Comprehensive Review.ACS pharmacology & translational science · 2024Review
- New Targets and Strategies for Rheumatoid Arthritis: From Signal Transduction to Epigenetic Aspect.Biomolecules · 2023Review
- Signaling pathways in rheumatoid arthritis: implications for targeted therapy.Signal transduction and targeted therapy · 2023Review
- Promising Therapeutic Targets for Treatment of Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes.Nature reviews. Rheumatology · 2020Review
- Histone methylation and acetylation in macrophages as a mechanism for regulation of inflammatory responses.Journal of cellular physiology · 2018Review
- A Novel In Vitro Human Granuloma Model of Sarcoidosis and Latent Tuberculosis Infection.American journal of respiratory cell and molecular biology · 2017Article
- Epigenetics in the pathogenesis of RA.Seminars in immunopathology · 2017Review
- Review
- Withaferin A induces cell death and differentiation in multiple myeloma cancer stem cells.MedChemComm · 2017Article
- Bruceantin inhibits multiple myeloma cancer stem cell proliferation.Cancer biology & therapy · 2016Article
- Suberoylanilide Hydroxamic Acid, an Inhibitor of Histone Deacetylase, Induces Apoptosis in Rheumatoid Arthritis Fibroblast-Like Synoviocytes.Inflammation · 2016Article
- Histone deacetylase inhibition activates Nrf2 and protects against osteoarthritis.Arthritis research & therapy · 2015Article
- Epigenetic mechanisms in cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study is to investigate the therapeutic effects of a novel histone deacetylase inhibitor (HDACi), NK-HDAC-1, on collagen-induced arthritis (CIA) and pathogenic fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). The proliferation and apoptosis of FLSs treated with NK-HDAC-1 were evaluated by flow cytometry and fluorescence staining. The effect of NK-HDAC-1 treatment on pro-inflammatory cytokine production was determined by ELISA. CIA was established in DBA/1 mice, and NK-HDAC-1 or vehicle was administered daily after the onset of arthritis. Clinical and histological scores were calculated to assess the therapeutic efficacy of NK-HDAC-1. NK-HDAC-1 significantly inhibited the proliferation of FLSs through cell cycle arrest at the G2/M checkpoint and enhanced apoptosis of FLSs. The activity of caspases was increased during NK-HDAC-1 treatment. IL-6 production by FLSs was also suppressed by NK-HDAC-1. Furthermore, the oral administration of NK-HDAC-1 significantly enhanced synoviocyte apoptosis in vivo and inhibited CIA progression. Compared with subcroylanilide hydroxamic acid which exhibited moderate prophylactic efficacy, NK-HDAC-1 demonstrated therapeutic efficacy in CIA. NK-HDAC-1 is a novel HDACi that may ameliorate inflammatory arthritis by regulating the activation, apoptosis, and inflammatory responses of FLSs. This is the first study to support that NK-HDAC-1 may be a potential therapeutic agent for RA.
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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.