Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

Table 1 Mechanisms and consequences related to protein kinase C activation-mediated harmful effects in diabetes mellitus

Reduction of nitric oxide production

Increased endothelin-1, prostaglandin E2 and thromboxane A2

Induction of growth factor expression: Transforming growth factor-β and vascular endothelial growth factor

Accumulation of microvascular matrix, fibronectin and type IV collagen

Overexpression of fibrinolytic inhibitor plasminogen activator inhibitor-1

Activation of the transcription factor nuclear factor kappa B

Increased nicotinamide adenine dinucleotide phosphate oxidase activity

Blood-flow abnormalities

Alteration of vascular permeability

Induction of angiogenesis

Organ fibrosis

Capillary occlusion

Induction of inflammatory mediators

Stimulation of oxidative stress