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]