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. 2014 Nov 11;2014:487097. doi: 10.1155/2014/487097

Table 1.

The pathogenesis of DN.

Genetic predisposition Renal hemodynamic changes [37]
 ACE genetic polymorphism [38]  Vasoactive hormones
 MTH-FR genetic polymorphism [38]  Systemic and intraglomerular pressure
 AGT genetic polymorphism [39]  Activation of RAAS
 Apolipoprotein E genetic polymorphism [40] Oxidative stress [41]
 Nicotinamide adenine dinucleotide phosphate (NADPH)
 Aldose reductase (ALR2) genetic polymorphism [42]
 Reactive oxygen species (ROS)
 Genetic locus 10p15.3, 7q21.3, 18q22.3, 14q23.1 [43]  Glucose-6-phosphate dehydrogenase (G6PDH)
Inflammatory reaction [44]
Abnormal glucose metabolism [45]  C-reactive protein (CRP) [46]
 Advanced glycation end products (AGEs) formation  Intercellular adhesion molecule (ICAM)
 Interleukin-1 (IL-1)
 Monocyte chemotactic protein-1 (MCP 1)
 Hexosamine pathways increased  Tumor necrosis factor-α (TNF-α)
 Polyol pathway flux increased Cytokine
 Protein kinase C (PKC) activation  Connective tissue growth factor (CTGF) [47]
Renal lipid accumulation  Insulin-like growth factor-I (IGF) [48]
 Adenosine monophosphate activated protein kinase (AMPK) [49]  Transforming growth factor-β (TGF-β) [50]
 Sterol regulatory element-binding protein (SREBP) [51]  Vascular endothelial growth factor (VEGF) [52]