Research advances in class Ⅰ histone deacetylases in chronic respiratory diseases

Liu Xiyue; Xue Xiaoli; Li Fangwei

doi:10.13406/j.cnki.cyxb.003601

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Research advances in class Ⅰ histone deacetylases in chronic respiratory diseases

Review | 更新时间：2025-10-23

- Research advances in class Ⅰ histone deacetylases in chronic respiratory diseases
- Journal of Chongqing Medical University Vol. 49, Issue 10, Pages: 1051-1054(2024)
- 作者机构：
  
  兰州大学第二医院呼吸内科，兰州 730000
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.003601
  CLC： R562.2
- Received：12 October 2023，
  
  Revised：2024-02-20，
  
  Accepted：07 March 2024，
  
  Published：28 October 2024
- 稿件说明：
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刘喜悦,薛小丽,李芳伟.Ⅰ类HDAC在慢性呼吸系统疾病中的研究进展[J].重庆医科大学学报,2024,49(10):1051-1054.

Liu Xiyue,Xue Xiaoli,Li Fangwei.Research advances in class Ⅰ histone deacetylases in chronic respiratory diseases[J].Journal of Chongqing Medical University,2024,49(10):1051-1054.
刘喜悦,薛小丽,李芳伟.Ⅰ类HDAC在慢性呼吸系统疾病中的研究进展[J].重庆医科大学学报,2024,49(10):1051-1054. DOI： 10.13406/j.cnki.cyxb.003601.

Liu Xiyue,Xue Xiaoli,Li Fangwei.Research advances in class Ⅰ histone deacetylases in chronic respiratory diseases[J].Journal of Chongqing Medical University,2024,49(10):1051-1054. DOI： 10.13406/j.cnki.cyxb.003601.

摘要

组蛋白的乙酰化及去乙酰化修饰在许多的病理生理过程中起重要作用，与许多疾病的发生发展密切相关。此修饰过程是动态可逆的，由组蛋白乙酰化酶（histone acetyltransferase，HAT）与组蛋白去乙酰化酶（histone deacetylase，HDAC）共同催化完成。不同亚型的HDAC通过不同的机制参与疾病的发生发展。慢性呼吸系统疾病是造成非传染性疾病巨大负担的重要因素，但是缺乏根治的方法。支气管哮喘、慢性阻塞性肺疾病、间质性肺疾病、肺动脉高压是最常见的慢性呼吸系统疾病，已有研究证实Ⅰ类HDAC在上述4种疾病的发病过程中起重要作用。本文通过对Ⅰ类HDAC在这4种疾病中的分子机制的研究进行综述，为其治疗提供新思路和靶点。

Abstract

The acetylation and deacetylation modifications of histones play an important role in many pathophysiological processes and are closely associated with the development and progression of many diseases. This modification process is dynamic and reversible is jointly catalyzed by histone acetylase and histone deacetylase（HDAC）. Different subtypes of HDAC participate in the development and progression of diseases through different mechanisms. Chronic respiratory diseases are an important factor causing the huge burden of non-communicable diseases，but there is still a lack of radical treatment methods. Bronchial asthma，chronic obstructive pulmonary disease，interstitial lung disease，and pulmonary hypertension are the most common chronic respiratory diseases，and studies have confirmed that class I HDACs play an important role in the pathogenesis of the above four diseases. This article reviews the research advances in the molecular mechanism of class I HDACs in these four diseases，so as to provides new ideas and targets for treatment.

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references

Bisserier M ， Janostiak R ， Lezoualc'h F ， et al . Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease [J ] . Vasc Biol ， 2020 ， 2 （ 1 ）： 17 - 34 .

Chronic Respiratory Disease Collaborators GBD . Prevalence and attributable health burden of chronic respiratory diseases，1990-2017：a systematic analysis for the Global Burden of Disease Study 2017 [J ] . Lancet Respir Med ， 2020 ， 8 （ 6 ）： 585 - 596 .

Choi JH ， Oh SW ， Kang MS ， et al . Trichostatin A attenuates airway inflammation in mouse asthma model [J ] . Clin Exp Allergy ， 2005 ， 35 （ 1 ）： 89 - 96 .

Ito K ， Caramori G ， Lim S ， et al . Expression and activity of histone deacetylases in human asthmatic airways [J ] . Am J Respir Crit Care Med ， 2002 ， 166 （ 3 ）： 392 - 396 .

Su XM ， Ren Y ， Li ML ， et al . Performance evaluation of histone deacetylases in lungs of mice exposed to ovalbumin aerosols [J ] . J Physiol Pharmacol ， 2018 ， 69 （ 2 ）： 26402 .

Peng XR ， Huang MY ， Zhao WQ ， et al . RAGE mediates airway inflammation via the HDAC1 pathway in a toluene diisocyanate-induced murine asthma model [J ] . BMC Pulm Med ， 2022 ， 22 （ 1 ）： 61 .

Lai TW ， Wu MD ， Zhang C ， et al . HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice [J ] . Am J Physiol Lung Cell Mol Physiol ， 2019 ， 316 （ 1 ）： 269 - 279 .

Li ML ， Su XM ， Ren Y ， et al . HDAC8 inhibitor attenuates airway responses to antigen stimulus through synchronously suppressing galectin-3 expression and reducing macrophage-2 polarization [J ] . Respir Res ， 2020 ， 21 （ 1 ）： 62 .

Masjedy A ， Salesi M ， Ahmadi A ， et al . Association between single-nucleotide polymorphism of cytokines genes and chronic obstructive pulmonary disease：a systematic review and meta-analysis [J ] . Cytokine ， 2023 ， 171 ： 156352 .

Tan CT ， Xuan LL ， Cao SH ， et al . Decreased histone deacetylase 2 （HDAC2） in peripheral blood monocytes（PBMCs） of COPD patients [J ] . PLoS One ， 2016 ， 11 （ 1 ）： e0147380 .

Mercado N ， Thimmulappa R ， Thomas CMR ， et al . Decreased histone deacetylase 2 impairs Nrf2 activation by oxidative stress [J ] . Biochem Biophys Res Commun ， 2011 ， 406 （ 2 ）： 292 - 298 .

Hodge G ， Jersmann H ， Tran HB ， et al . Lymphocyte senescence in COPD is associated with decreased histone deacetylase 2 expression by pro-inflammatory lymphocytes [J ] . Respir Res ， 2015 ， 16 （ 1 ）： 130 .

Lai TW ， Tian BP ， Cao C ， et al . HDAC2 suppresses IL17A-mediated airway remodeling in human and experimental modeling of COPD [J ] . Chest ， 2018 ， 153 （ 4 ）： 863 - 875 .

Winkler AR ， Nocka KN ， Williams CMM . Smoke exposure of human macrophages reduces HDAC3 activity，resulting in enhanced inflammatory cytokine production [J ] . Pulm Pharmacol Ther ， 2012 ， 25 （ 4 ）: 286 - 292 .

Zhang M ， Hei R ， Zhou Z ， et al . Macrophage polarization involved the inflammation of chronic obstructive pulmonary disease by S1P/HDAC1 signaling [J ] . Am J Cancer Res ， 2023 ， 13 （ 9 ）： 4478 - 4489 .

Racanelli AC ， Kikkers SA ， Choi AMK ， et al . Autophagy and inflammation in chronic respiratory disease [J ] . Autophagy ， 2018 ， 14 （ 2 ）： 221 - 232 .

Saito S ， Zhuang Y ， Suzuki T ， et al . HDAC8 inhibition ameliorates pulmonary fibrosis [J ] . Am J Physiol Lung Cell Mol Physiol ， 2019 ， 316 （ 1 ）： 175 - 186 .

Chen F ， Gao Q ， Zhang LJ ， et al . Inhibiting HDAC3（histone deacetylase 3） aberration and the resultant Nrf2（nuclear factor erythroid-derived 2-related factor-2） repression mitigates pulmonary fibrosis [J ] . Hypertension ， 2021 ， 78 （ 2 ）： 15 - 25 .

Korfei M ， Skwarna S ， Henneke I ， et al . Aberrant expression and activity of histone deacetylases in sporadic idiopathic pulmonary fibrosis [J ] . Thorax ， 2015 ， 70 （ 11 ）： 1022 - 1032 .

Rubio K ， Singh I ， Dobersch S ， et al . Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis [J ] . Nat Commun ， 2019 ， 10 ： 2229 .

Toscano-Marquez F ， Romero Y ， Espina-Ordoñez M ， et al . Absence of HDAC3 by matrix stiffness promotes chromatin remodeling and fibroblast activation in idiopathic pulmonary fibrosis [J ] . Cells ， 2023 ， 12 （ 7 ）： 1020 .

Rabinovitch M . Molecular pathogenesis of pulmonary arterial hypertension [J ] . J Clin Invest ， 2012 ， 122 （ 12 ）： 4306 - 4313 .

Li M ， Riddle SR ， Frid MG ， et al . Emergence of fibroblasts with a proinflammatory epigenetically altered phenotype in severe hypoxic pulmonary hypertension [J ] . J Immunol ， 2011 ， 187 （ 5 ）： 2711 - 2722 .

Yang QW ， Sun M ， Ramchandran R ， et al . IGF-1 signaling in neonatal hypoxia-induced pulmonary hypertension：role of epigenetic regulation [J ] . Vascul Pharmacol ， 2015 ， 73 ： 20 - 31 .

Nozik-Grayck E ， Woods C ， Stearman RS ， et al . Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension [J ] . Am J Physiol Lung Cell Mol Physiol ， 2016 ， 311 （ 1 ）： 124 - 134 .

Yu QJ ， Tai YY ， Tang Y ， et al . BOLA（BolA family member 3） deficiency controls endothelial metabolism and glycine homeostasis in pulmonary hypertension [J ] . Circulation ， 2019 ， 139 （ 19 ）： 2238 - 2255 .

Li FW ， Wang D ， Wang H ， et al . Inhibition of HDAC1 alleviates monocrotaline-induced pulmonary arterial remodeling through up-regulation of miR-34a [J ] . Respir Res ， 2021 ， 22 （ 1 ）： 239 .

Chelladurai P ， Dabral S ， Basineni SR ， et al . Isoform-specific characterization of class Ⅰ histone deacetylases and their therapeutic modulation in pulmonary hypertension [J ] . Sci Rep ， 2020 ， 10 （ 1 ）： 12864 .

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