From: The role of cigarette smoke-induced epigenetic alterations in inflammation
Genes/CpG sites | Changes by CS | Functions on inflammation | Mechanism | Disease | References | Year |
---|---|---|---|---|---|---|
RUNX3 | Hypermethylation [107] | Pro-inflammation | Associated with the level of CRP | COPD | Siedlinski et al. [107] | 2012 |
JAK3 | Hypermethylation [107] | Pro-inflammation | Associated with the level of CRP | COPD | Siedlinski et al. [107] | 2012 |
KRT1 | Hypermethylation [107] | Pro-inflammation | Associated with the level of CRP | COPD | Siedlinski et al. [107] | 2012 |
cg18181703 in SOCS3 | N/A | Anti-inflammation | Hypomethylation of the CpG site was associated with higher CRP levels | CHD | Ligthart et al. [108] | 2016 |
cg06126421 in TUBB | N/A | Anti-inflammation | Hypomethylation of the CpG site was associated with higher CRP levels | CHD | Ligthart et al. [108] | 2016 |
cg05575921 in AHRR | Hypomethylation [109] | Anti-inflammation | Hypomethylation of the CpG site was associated with higher CRP levels | CHD | Ligthart et al. [108] | 2016 |
cg03636183 in F2RL3 | Hypomethylation [110] | Pro-inflammation | Increase IL-18 levels | Hypertension | Jhun et al. [110] | 2017 |
DNMT1 | Upregulation [27] | Pro-inflammation | Increase methylation level of the PPAR-γ promoter and reduce expression of PPAR-γ | Atherosclerosis | Yu et al. [113] | 2016 |
DNMT1 | Upregulation [27] | Pro-inflammation | Regulates IL-6 and TGFβ1; meanwhile, be activated by IL-6 and TGFβ | Benign prostatic hyperplasia | Xu et al. [117] | 2017 |
DNMT1 | Upregulation [27] | Pro-inflammation | Be activated by IL-1β via MAPK and NF-κB pathways. | Benign meningiomas | Wang et al. [118] | 2016 |
TET1 | N/A | Pro-inflammation | TET1 knockdown reduced IL-6 and TNF-α levels through downregulating NF-κB signaling pathway | Periodontal diseases | Huang et al. [119] | 2019 |
TET2 | N/A | Pro-inflammation | Activate the NF-κB signaling pathway | Dental pulp inflammation | Wang et al. [120] | 2018 |