ArticleJournal of translational medicine2025
Inhibition of histone deacetylases 3 attenuates imiquimod-induced psoriatic dermatitis via targeting cGAS-STING signaling in keratinocytes.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Antitumor activity and structure-activity relationship of poly (ADP-ribose) polymerase (PARP)-based dual inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Experimental Validation of an Immune Cell Infiltration Signature in Psoriasis: Translating Computational Modeling to In Vivo Efficacy.Journal of clinical laboratory analysis · 2026Article
- Obesity is the culprit behind fatty acid-induced inflammation.Nutrition & metabolism · 2026Review
- HDAC3 Mediates Hippocampal Microglial Pyroptosis Via the STING/NLRP3 Pathway and Contributes To Cognitive Impairment in Sepsis-Associated Encephalopathy.Inflammation · 2026Article
- Long Noncoding RNA MIR205HG Elevates FSTL1 Expression to Drive Calcium Oxalate Nephrolithiasis in vitro through Absorbing miR-5581-3p.Kidney & blood pressure research · 2026Article
- The role of protein lactylation in skin diseases: from molecular mechanisms to potential therapeutics.Frontiers in immunology · 2026Review
- The multifaceted role of NF-κB signaling in psoriasis: from inflammatory amplification to epidermal remodeling.Frontiers in immunology · 2026Review
- Recent Insights into the Creation of Histone Deacetylase Inhibitors for the Treatment of Human Diseases.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundPsoriasis is a common chronic inflammatory skin disease characterized by epidermal keratinocyte hyperproliferation and persistent immune activation. Histone deacetylase 3 (HDAC3), a member of the class I HDAC family, plays critical roles in regulating immunity and inflammation. However, its precise expression profile and functional contribution to psoriasis pathogenesis remain poorly defined.
methodsWe first performed bioinformatics analysis of HDAC3 expression using the Gene Expression Omnibus (GEO) database. Subsequently, we employed a combination of cellular and molecular techniques, including hematoxylin and eosin (H&E) staining, immunohistochemistry, flow cytometry, quantitative real-time PCR (qRT-PCR), western blotting, and transmission electron microscopy (TEM), to analyze the role of HDAC3 in IMQ-induced psoriasis-like inflammation in mice and in vitro psoriasis models.
resultsHDAC3 expression was significantly upregulated in psoriasis lesions of patients and in both in vitro and in vivo models of psoriasis. Pharmacological inhibition of HDAC3 using the specific inhibitor RGFP966 alleviated IMQ-induced skin inflammation in mice and suppressed psoriasis-like phenotypes in vitro. Mechanistically, HDAC3 upregulation in an inflammatory microenvironment promoted oxidative stress, disrupted mitochondrial structural integrity, and triggered mitochondrial DNA leakage into the cytosol, thereby activating the cGAS-STING pathway in keratinocytes.
conclusionOur findings establish HDAC3 as a pivotal mediator of psoriasis pathogenesis through the cGAS-STING pathway via mitochondrial dysfunction. The role of HDAC3 in exacerbating epidermal hyperproliferation and inflammation highlights its potential as a therapeutic target. Targeting HDAC3 in keratinocytes may offer a novel strategy for preventing and treating psoriasis by modulating epigenetic regulation, mitochondrial homeostasis, and innate immune responses.
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