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Role of NF-Kappa B (NF-κB) in Diabetes

Volumen 4, Ausgabe 2, 2013, pp. 111-132
DOI: 10.1615/ForumImmunDisTher.2013008396
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ABSTRAKT

NF kappa B (NF-κB) plays a central and crucial role in the development of diabetes mellitus (DM) and various complications associated with DM. In DM, the NF-κB is activated by a number of pro-inflammatory cytokines, to regulate both survival and death of β-cells, but it is predominantly pro-apoptotic in β-cells. The activation of inducible nitric oxide synthase gene expression and subsequent formation of nitric oxide is also partly involved in the destruction of β-cells. In type 1 diabetes (T1D), interleukin-1 β-induced NF-κB activation causes the apoptosis of β-cells in the pancreas. However, in type 2 diabetes, activated NF-κB induces both apoptosis and insulin resistance. Reactive oxygen species and advanced glycation end products (AGEs) contribute to the progression of a variety of micro- and macro-complications of DM. The interactions of AGEs and their receptor RAGE also lead to the upregulation of NF-κB. Sustained activation of NF-κB induces the systemic inflammation, which is a contributory factor for the development of various diabetic ailments. There are evidences for the activation and involvement of NF-κB in all major diabetic complications such as diabetic cardiomyopathy, retinopathy, nephropathy, and neuropathy. Hence, an NF-κB-based therapeutic approach should be developed for DM. Several antioxidants, including flavonoids, seem to be promising candidates.

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