Table 3 Studies reporting aberrant HATs/HDACs induced by CS in inflammation
From: The role of cigarette smoke-induced epigenetic alterations in inflammation
HATs/HDACs | Changes by CS | Functions on inflammation | Mechanism | Disease | References | Year |
|---|---|---|---|---|---|---|
CBP/p300 | Upregulation [50] | Pro-inflammation | Increase acetylation of histones (H3/H4) and NF-κB | COPD | Rajendrasozhan et al. [126] | 2009 |
HDAC1 | Downregulation [37] | Anti-inflammation | Decrease level of acetylated H3K9 | COPD | Chen et al. [37] | 2015 |
HDAC2 | Anti-inflammation | Inhibit IL-17A Suppress the phosphorylation of Akt Inhibit NF-κB | COPD Asthma COPD | Lai et al. [127] Xia et al. [128] To et al. [129] | 2018 2018 2017 | |
HDAC3 | Anti-inflammation | Repress synthesis of NF-κB -driven inflammatory cytokine | COPD | Winkler et al. [40] | 2012 | |
HDAC4 | Downregulation [38] | Anti-inflammation | Repress c-Jun and IL-17A | COPD | Lu et al. [134] | 2015 |
HDAC5 | Pro-inflammation | Activate NF-κB | Chronic inflammatory diseases Mycoplasma pneumoniae pneumonia | Poralla et al. [135] Zhao et al. [136] | 2015 2019 | |
HDAC6 | Upregulation [41] Activation [42] | Pro-inflammation | Promote the increase of matrix metalloproteinase 9 expression and activate NF-κB by inducing IĸB phosphorylation Promote the phosphorylation of p38 MAPK | Acute lung injury Brain inflammation | Liu et al. [137] Song et al. [138] | 2019 2019 |
HDAC7 | Downregulation [35] | Anti-inflammation | Increase histone deacetylation of memory T lymphocytes | Asthma | Zhang et al. [139] | 2015 |
HDAC8 | Anti-inflammation Pro-inflammation | Promote the acetylation modification of IFNβ1 promoter, thus selectively increasing innate IFN-β production Increase the production of IL-1β, TNFα, and IL-6 | Asthma Systemic juvenile idiopathic arthritis | Meng et al. [140] Li et al. [141] | 2016 2015 | |
HDAC9 | N/A | Anti-inflammation | Increase histone deacetylation of memory T lymphocytes | Asthma | Zhang et al. [139] | 2015 |
HDAC10 | Downregulation [36] | Anti-inflammation | Increase histone deacetylation of memory T lymphocytes | Asthma | Zhang et al. [139] | 2015 |
HDAC11 | N/A | Anti-inflammation | Increase histone deacetylation of memory T lymphocytes | Asthma | Zhang et al. [139] | 2015 |
SIRT1 | Downregulation [43] | Anti-inflammation | Deacetylate the RelA/p65 subunit of NF-κβ and attenuate NF-κB-mediated gene transcription | Chronic inflammatory diseases | Schug et al. [145] | 2010 |
SIRT2 | N/A | Anti-inflammation | Deacetylate the RelA/p65 subunit of NF-κB at Lys310 and inhibit NF-κβ signaling | Inflammatory bowel disease | Lo et al. [146] | 2014 |
SIRT3 | Downregulation [46] | Anti-inflammation | Ameliorate NLRP3 inflammasome activation Decrease the expression levels of NF-κB, HMGB1, c-Jun, c-Fos, COX2, TNF-α, IL-1β and IL-6 | Hyperlipidaemia Chronic kidney disease | Liu et al. [148] Qiao et al. [149] | 2018 2018 |
SIRT4 | Downregulation [47] | Anti-inflammation | Suppress NF-κB activating via inhibiting the degradation of IκBα | COPD | Chen et al. [47] | 2014 |
SIRT5 | Downregulation [48] | Pro-inflammation | Compete with SIRT2 to interact with NF-κB p65 to block the deacetylation of p65 by SIRT2, leading to increased acetylation of p65 and the activation of NF-κB pathway | Sepsis | Qin et al. [151] | 2017 |
SIRT6 | Downregulation [49] | Anti-inflammation | Interact with p65/RelA bound to the NF-κβ promoter region and repress transcriptional activity | Inflammatory vascular diseases | Lappas M. [147] | 2012 |
SIRT7 | N/A | Anti-inflammation | Deacetylate p53, leading to inactivation of p53 | Heart diseases | Vakhrusheva et al. [150] | 2008 |