Ask about this productRelated genes to: HDAC11 antibody
- Gene:
- HDAC11 NIH gene
- Name:
- histone deacetylase 11
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-09
- Date modifiied:
- 2014-11-19
Related products to: HDAC11 antibody
Related articles to: HDAC11 antibody
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is frequently accompanied by hepatic fibrosis and systemic cardiovascular complications; however, the mechanistic interplay between coagulation abnormalities and disease progression remains poorly defined. Here, analyses of liver tissues and plasma from patients with MASLD, together with complementary mouse models, suggest an important role of immunothrombosis in fibrotic progression. In MASLD mouse models, pharmacological anticoagulation with dabigatran or aspirin attenuates fibrosis but increases systemic bleeding risk, highlighting the need for more selective strategies. Mechanistically, neutrophil extracellular traps (NETs) promote localized fibrin deposition within the hepatic microvasculature, leading to impaired microcirculation and liver sinusoidal endothelial cell (LSEC) capillarization associated with increased Piezo1-dependent mechanosensation, thereby exacerbating fibrosis. Further investigation identifies neutrophil-derived fibrinogen-like protein 2 (FGL2) as a key upstream regulator of NETs formation through interaction with histone deacetylase 11 (HDAC11), promoting histone H3 deacetylation and facilitating PAD4-mediated citrullination to drive NETs release. Genetic disruption of FGL2 or NETs inhibition restores LSEC fenestration, improves microvascular hemodynamics, and attenuates fibrosis without increasing systemic bleeding risk. Together, these findings define an immunothrombotic axis linking neutrophil-derived FGL2-HDAC11 signaling to NETs formation and endothelial dysfunction in MASLD, providing mechanistic insight into the interplay between coagulation and metabolic liver disease. - Source: PubMed
Publication date: 2026/05/10
Li XitangHu JunjianHai SupingHu PengWu WenhuiGao QiangYu BinghuiXu FeiyangZheng XizheGuan QiantingXiang HuilingXi DongYan WeimingWang PengZhang Bin-HaoNing QinWang Xiaojing - Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease where macrophages drive fibrogenesis, yet Hdac11's role is unclear. We first identify pronounced Hdac11 upregulation in IPF lungs, which is associated with an enrichment in alveolar macrophages (AMs). Genetic ablation of Hdac11 or adoptive transfer of Hdac11-deficient macrophages markedly attenuates fibrosis. Specifically, Hdac11 deficiency significantly reduces M2 macrophage polarization in vivo and vitro and is associated with reduced macrophage-myofibroblast transition (MMT) like phenotypic reprogramming, thereby decreasing myofibroblast accumulation and profibrotic gene expression. Mechanistically, impaired mitophagy mediates Hdac11-mediated M2 macrophage polarization and is associated with MMT-like changes. Hdac11 regulates mitochondrial quality control by deacetylating Parkin at lysine 76, promoting its ubiquitination and degradation, which impairs mitophagy and drives profibrotic macrophage activation. Pharmacological Hdac11 inhibition effectively reverses bleomycin-induced fibrosis. Taken together, our work identifies Hdac11 as a target of Parkin-mediated mitophagy in macrophages, establishing Hdac11-Parkin axis disruption as an important mechanism in IPF and highlighting Hdac11 inhibition as a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/04/17
Nie YunjuanXu LiLiu YanyanLi JiaoWang ZhixuZhai XiaorunSun XiaoruHu ChunxiaoXu BoWu YaxianYu HaitaoKarpurapu ManjulaGuo HuaqiChai Gaoshang - Mood stabilizers (MS) are the cornerstone of maintenance treatment for bipolar disorder. However, their mechanisms of action remain only partially understood. Increasing evidence suggests that MS may exert part of their therapeutic effects through epigenetic modulations. In this exploratory study, we investigated the effects of therapeutic concentrations of six MS - valproic acid (VPA), lithium, lamotrigine, risperidone, aripiprazole, and quetiapine - on the expression of 82 genes involved in DNA methylations and histone modifications in HeLa cells. After seven days of exposure, VPA induced the most extensive transcriptional changes, with differential expression of 17 out of 82 genes, predominantly involved in histone modifications (acetylation, methylation, phosphorylation, ubiquitination). Notably, VPA upregulated HDAC1, HDAC2, HDAC9, HDAC11, KDM5B, and PAK1 mRNA levels with fold-changes >1.3. Corresponding increased protein levels were observed only for KDM5B and PAK1. VPA also induced direct inhibition of total HDAC activity, unlike lithium and quetiapine. Lithium and quetiapine upregulated HDAC2 and ESCO1 mRNA levels. Lithium and quetiapine did not modify HDAC2 protein levels. Other MS showed no significant transcriptional effects at day 7. Overall, MS-induced transcriptional changes were mainly restricted to genes involved in histone modifications, with minimal effects on DNA methylation-related genes. These findings suggest that MS, particularly VPA, modulate the transcription of epigenetic machinery genes in HeLa cells. HDAC2 upregulation may represent a shared transcriptional response across several MS, although the absence of consistent protein-level changes warrants caution. These results are exploratory and require replication in more physiologically relevant models to determine their biological and clinical significance. - Source: PubMed
Publication date: 2026/04/08
Hennion VincentRathes ArthnaPuszkiel AlicjaBellivier FrankDecleves XavierFroelicher-Bournaud LéoEtain BrunoMarie-Claire Cynthia - Our previous study not only demonstrated that HDAC11 is a potential therapeutic target for AML but also discovered a specific HDAC11 inhibitor as an anti-AML lead compound. The purpose of the present study was to discover novel specific HDAC11 inhibitors with improved drug-like properties through structural modification and optimization of . Among the newly synthesized derivatives, compound stood out as a potent and specific HDAC11 inhibitor with desirable liver microsomal stability. Notably, compared with the well-known HDAC11 inhibitor FT895, compound exhibited much stronger multiple anti-AML effects including proliferation inhibition, apoptosis induction, cell cycle arrest, differentiation promotion, and ferroptosis induction. Moreover, combination of and ivosidenib, an approved targeted therapeutic drug for AML, showed strong synergistic anti-AML potency. Satisfyingly, compound exhibited acceptable oral pharmacokinetic parameters in mouse, which supported its robust oral anti-AML potency in an MLL-AF9-induced mouse AML model, both alone and in combination with ivosidenib. - Source: PubMed
Publication date: 2026/03/05
Chai QipengYang MaoshuoLiu ChunxiZhu XiaolanLiu LinaZhao WeiXue XintongZhang JinweiLiu LanlanWang WenjingLiu FabaoYou XiaonaZhang Yingjie - Histone deacetylases (HDACs), as key epigenetic regulators, serve a central role in tumorigenesis and progression by modulating chromatin architecture and gene transcription. In recent years, notable advances have been made in elucidating the pan-cancer mechanisms of HDACs and their inhibitors (HDACis), as well as in performing clinical studies, with their antitumor activity becoming a major research focus. The present review summarized the classification and molecular mechanisms of HDACs alongside their roles in various malignancies including ovarian cancer, endometrial carcinoma, glioma, osteosarcoma and multiple myeloma. The present review specifically elaborated on the relationship between particular isoforms, such as HDAC3, HDAC5, HDAC7 and HDAC11, and tumor progression, detailing associated signaling pathways. The present review systematically evaluated the current clinical applications of HDACis, examining both monotherapy and combination therapy efficacy alongside existing challenges. Furthermore, the present review discussed recent progress in structural modifications aimed at enhancing selectivity while reducing toxicity, as well as novel targeting strategies. Concluding with perspectives on HDAC-based therapies, the present review underscores the key importance of precision targeting and combinatorial approaches to improve patient outcomes in the future. - Source: PubMed
Publication date: 2026/02/24
Lin RunlingZhang YuLi HongLiang Fan