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. 2020 Sep 25;21(19):7057. doi: 10.3390/ijms21197057

Figure 2.

Figure 2

Oxidative stress and ER stress in inflammation in DKD. In oxidative stress, HG activates the overproduction of AGE and PKC, mitochondria damage and NOX4, which promotes the generation of ROS to induce inflammation by the upregulation of TXNIP, p38MAPK signalling pathway and NF-κB signalling pathway. In ER stress, disruption of homeostasis between the ER and mitochondria and NADPH oxidase in ER activates NF-κB signalling pathway by ROS overproduction. In inflammation, pathways above activate NLRP3 inflammasome and caspase-1 and induce secretion of IL-18 and IL-1β. PKC, protein kinase C; AGE, advanced glycosylation end product; NOX4, NADPH oxidases 4; ROS, reactive oxygen species; XNIP, thioredoxin interacting protein; TRX, thioredoxin; NF-κB, nuclear transcription factor; MAPK, mitogen-activated protein kinase.