Guidance Cue Netrin-1 and the Regulation of Inflammation in Acute and Chronic Kidney Disease

Figure 1

Inflammation in acute kidney injury. Ischemia reperfusion or nephrotoxin causes tubular epithelial stress or necrosis which releases inflammatory mediators. These inflammatory mediators activate endothelial cells and expression of adhesion molecules (II) such as ICAM-1 induces leukocyte migration into the interstitium and release of vasoconstrictor. At the same time inflammation downregulates anti-inflammatory molecules such as netrin-1 and endothelial nitric oxide. Infiltrated white blood cells such as neutrophils, monocyte, and T cells release cytokine, chemokines, proteases, and oxygen radicals cause further damage to the epithelium. All these events lead to vasoconstriction and persistent hypoxia which contributes to further tissue damage.