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. 2023 Oct 4;14:1232790. doi: 10.3389/fendo.2023.1232790

Figure 2.

Figure 2

NF-κB signaling pathway in the pathogenesis of DKD. Activation of NF-κB is tightly regulated by the IκB regulatory protein family. This regulation occurs through the phosphorylation of the inhibitory protein IκB kinase by specific IκB proteins, followed by its degradation via proteolysis. Once freed, NF-κB translocates from the cytoplasm into the nucleus. Within the nucleus, NF-κB binds to specific promoter and enhancer sites on target genes, initiating the process of transcription. This activation leads to increased transcription of genes encoding inflammatory cytokines and other molecules associated with this complication As a result, renal inflammation is triggered due to the involvement of the NF-κB signaling pathway, ultimately contributing to the development of renal inflammation. IL-1R, Interleukin-1 Receptor; DAG, Diacylglycerol; PKC, Protein Kinase C; IkB, NF-kappa-B Inhibitor; FADD, Fas-associated with Death Domain Protein; TRADD, TNF Receptor 1 Associated via the Death Domain; TRAF2, TNF Receptor-Associated Factor 2; RIP, Receptor-interacting Protein; IKKs, IΚB Kinases; TOLLIP, Recombinant Toll Interacting IRAK, Interleukin Receptor-Associated Kinase; ACP, Acyl Carrier Protein; NIK, NF -κB Inducing Kinase; TAK1, Transforming Growth Factor Kinase 1; CTGF; Recombinant Connective Tissue Growth Factor; MyD88, Myeloid Differentiation Factor 88; HSP70, Heatshockprotein70; By Figdraw (www.figdraw.com).