الفهرس 
Diabetes mellitusOnly 14 pages are availabe for public view
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Abstract
Diabetic nephropathy (DN) is a principal cause of end-stage renal
disease in the world and a major cause of morbidity and mortality from diabetic complications (Kong et al.,2013).The major signaling mechanisms involved in the pathogenesis of DN include increasing levels of angiotensin II, formation of advanced glycation end-products (AGE),increasing activation of protein kinase c (PKC), and lipid accumulation (Balakumar et al. 2009) . chronic hyperglycemia is a major risk factor that activates all these signaling pathways involved in the development and progression of DN. Hyperglycemia leads to increased formation of AGE that interact with their receptors (RAGE), induce oxidative stress, and stimulate production/release of cytokines that help lead to increase
inflammation and tissue damage. Because oxidative stress and various AGE interact to up-regulate one another, this can lead to matrix accumulation and mesangial cell hypertrophy (Suzuki et al. 2006; Yuan et al. 2011). High glucose levels also help to elevate angiotensin II (Ang II) production (Singh et al. 2003) that, in turn, mediates pathophysiological changes in the kidney. As a pro-inflammatory peptide, Ang II also contributes to the induction/progression of glomerular inflammation and fibrosis (Gawaz et al. 2005; Tu et al. 2008). g II causes activation of NF-kB that then leads to increased transcription of trans-forming growth factor (TGF)-β1 and
inflammatory cytokines (King 2008). Ang II also activates NADPH oxidase, the major source of superoxide anions, leading to local oxidative stress (Balakumar et al. 2009).