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. 2022 Dec 30;2022:5774641. doi: 10.1155/2022/5774641

Figure 3.

Figure 3

The role of OGG1 in the regulation of inflammation and fibrosis. OGG1 can act as a positive regulator of NF-κB to prompt P50, P65, and TNF-α expression and further prompt the release of pro-IL-1β and the upstream inflammatory factors IL-1β. Furthermore, OGG1 regulates cGAS-STING pathway to increase the expression of the proinflammatory genes P50, P65, and PIRF3. Fibrosis is the main pathological process of various chronic diseases at the end stage and can be driven by inflammation. OGG1 can activate TGF-β to promote Smad2/3, notch, PI3K/AKT, and MAPK/mTOR signaling pathway and prompt the expression of fibrosis genes α-SMA, FN, and MMPs/TIMPs and downstream ZO-1. OGG1 can also positively regulate Wnt/β-catenin, VEGF, and CTGF, thus aggravating fibrosis. TNF-α: tumor necrosis factor-α; PIRF3: phosphointerferon regulatory factor 3; TGF-β: transforming growth factor beta; α-SMA: alpha-smooth muscle actin; FN: fibronectin; MMPs: matrix metalloproteinases; TIMPs: tissue inhibitors of metalloproteinases; ZO-1: zonula occludens-1. PI3K: phosphoinositide 3-kinase; MAPK: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; RTK: receptor tyrosine kinase.