Table 5 CS‐regulated lncRNAs and their role in inflammation
From: The role of cigarette smoke-induced epigenetic alterations in inflammation
LncRNAs | Changes by CS | Functions on inflammation | Mechanism | Disease | References | Year |
|---|---|---|---|---|---|---|
HOTAIR | Pro-inflammation | Promote TNF-α production by activating NF-κB signaling Promote the expression of protein kinase resource, TNF-α and IL-6 Promote the expression of IL‐6, IL‐1β, COX2, and TNF-α Upregulated by pro-inflammatory cytokine IL-6 | Sepsis Keratinocyte injury Atherosclerosis Lung cancer | Wu et al. [201] Liu and Zhang [203] Liu et al. [204] Liu et al. [101] | 2016 2018 2019 2015 | |
MALAT1 | Upregulation [103] | Pro-inflammation Anti-inflammation | Activate p38 MAPK/NF-κB Increase serum amyloid antigen 3 Upregulated by pro-inflammatory cytokine IL-6 Inhibit the DNA binding activity of NF-κB | Sepsis Diabetes Sepsis N/A | Chen et al. [205] Puthanveetil et al. [206] Zhuang et al. [208] Zhao et al. [207] | 2018 2015 2017 2016 |
CCAT1 | Upregulation [102] | Pro-inflammation | Trigger TNF-α, IFN-γ expression by targeting miR-185-3p, meanwhile upregulated by TNF-α | Inflammatory bowel disease | Ma et al. [209] | 2019 |