Copyright
©The Author(s) 2015.
World J Diabetes. May 15, 2015; 6(4): 598-612
Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.598
Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.598
Figure 3 Target genes activated by NF-κB.
TNF-α: Tumor necrosis factor-alpha; IFN-γ: Interferon-gamma; IL: Interleukin; TGF-β: Tumor growth factor-beta; MCP-1: Monocyte chemoattractant protein-1; MIP: Major intrinsic protein; TNFR: Tumor necrosis factor receptor; INFR: Interferon receptor; IL-R: Interleukin receptor; CD: Cluster of differentiation; ICAM: Intracellular cell adhesion molecule; VCAM: Vascular cell adhesion molecule; CCR: Chemokine CC receptor; TLR: Toll-like receptor; Lox: Lysyl oxidase; RAGE: Receptor advanced glycation end product; PAI: Plasminogen inhibitor activator; SAA: Serum amyloid; CRP: C-reactive protein; COX: Cyclo-oxygenase; iNOS: Inducible nitric oxide synthase; VEGF: Vascular endothelial growth factor; IGFBPs: Insulin-like growth factor binding protein; MnSOD: Manganese superoxide dismutase; RelA: Reticuloendotheliosis viral oncogene homolog A; NF-κB: Nuclear factor-kappa B; IKK: Inhibitor Kappa B kinase; IκBα: Inhibitor of NF-κB; TNFAIP3: TNF-α induced protein 3.
- Citation: Hameed I, Masoodi SR, Mir SA, Nabi M, Ghazanfar K, Ganai BA. Type 2 diabetes mellitus: From a metabolic disorder to an inflammatory condition. World J Diabetes 2015; 6(4): 598-612
- URL: https://www.wjgnet.com/1948-9358/full/v6/i4/598.htm
- DOI: https://dx.doi.org/10.4239/wjd.v6.i4.598