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Table 3 Studies reporting aberrant HATs/HDACs induced by CS in inflammation

From: The role of cigarette smoke-induced epigenetic alterations in inflammation

HATs/HDACsChanges by CSFunctions on inflammationMechanismDiseaseReferencesYear
CBP/p300Upregulation [50]Pro-inflammationIncrease acetylation of histones (H3/H4) and NF-κBCOPDRajendrasozhan et al. [126]2009
HDAC1Downregulation [37]Anti-inflammationDecrease level of acetylated H3K9COPDChen et al. [37]2015
HDAC2Downregulation [29, 30, 38]Anti-inflammationInhibit IL-17A
Suppress the phosphorylation of Akt
Inhibit NF-κB
Lai et al. [127]
Xia et al. [128]
To et al. [129]
HDAC3Downregulation [39, 40]Anti-inflammationRepress synthesis of NF-κB -driven inflammatory cytokineCOPDWinkler et al. [40]2012
HDAC4Downregulation [38]Anti-inflammationRepress c-Jun and IL-17ACOPDLu et al. [134]2015
HDAC5Downregulation [29, 30]Pro-inflammationActivate NF-κBChronic inflammatory diseases Mycoplasma pneumoniae pneumoniaPoralla et al. [135]
Zhao et al. [136]
HDAC6Upregulation [41]
Activation [42]
Pro-inflammationPromote 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]
HDAC7Downregulation [35]Anti-inflammationIncrease histone deacetylation of memory T lymphocytesAsthmaZhang et al. [139]2015
HDAC8Downregulation [29, 30]Anti-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
Systemic juvenile idiopathic arthritis
Meng et al. [140]
Li et al. [141]
HDAC9N/AAnti-inflammationIncrease histone deacetylation of memory T lymphocytesAsthmaZhang et al. [139]2015
HDAC10Downregulation [36]Anti-inflammationIncrease histone deacetylation of memory T lymphocytesAsthmaZhang et al. [139]2015
HDAC11N/AAnti-inflammationIncrease histone deacetylation of memory T lymphocytesAsthmaZhang et al. [139]2015
SIRT1Downregulation [43]Anti-inflammationDeacetylate the RelA/p65 subunit of NF-κβ and attenuate NF-κB-mediated gene transcriptionChronic inflammatory diseasesSchug et al. [145]2010
SIRT2N/AAnti-inflammationDeacetylate the RelA/p65 subunit of NF-κB at Lys310 and inhibit NF-κβ signalingInflammatory bowel diseaseLo et al. [146]2014
SIRT3Downregulation [46]Anti-inflammationAmeliorate NLRP3 inflammasome activation
Decrease the expression levels of NF-κB, HMGB1, c-Jun, c-Fos, COX2, TNF-α, IL-1β and IL-6
Chronic kidney disease
Liu et al. [148]
Qiao et al. [149]
SIRT4Downregulation [47]Anti-inflammationSuppress NF-κB activating via inhibiting the degradation of IκBαCOPDChen et al. [47]2014
SIRT5Downregulation [48]Pro-inflammationCompete 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 pathwaySepsisQin et al. [151]2017
SIRT6Downregulation [49]Anti-inflammationInteract with p65/RelA bound to the NF-κβ promoter region and repress transcriptional activityInflammatory vascular diseasesLappas M. [147]2012
SIRT7N/AAnti-inflammationDeacetylate p53, leading to inactivation of p53Heart diseasesVakhrusheva et al. [150]2008
  1. CBP cAMP-response element binding protein, COX2 cyclooxygenase-2, CS cigarette smoke, HAT histone acetyltransferases, HDACs histone deacetylases, HMGB1 high mobility group box 1, IFNβ1 interferon beta 1, IκBα inhibitory kappa B kinase α, IL interleukin, NLRP3 NOD-like receptor family, pyrin domain containing 3, SIRT sirtuin