Adenosine A1 Receptor Deficiency Aggravates Extracellular Matrix Accumulation in Diabetic Nephropathy through Disturbance of Peritubular Microenvironment

Figure 8

Microvascular pericytes in normal and injured kidneys. (a) In a healthy kidney, the pericytes of microvascular expressed PDGFRβ closely contact with endothelial cells, maintaining proper endothelial function and microvascular integrity. (b) In the diabetic kidney, hyperglycemia activates microvascular pericytes to detach from the endothelial cells. Then, pericytes differentiated to myofibroblasts and migrated into the interstitium to produce large amounts of collagen, inducing pathologic extracellular matrix deposition. Consistent injury leads to unstable vasculature, capillary loss, interstitial matrix expansion, and tubular interstitial fibrosis. A1AR, widely distributed in the renal proximal tubule, interstitial, and vascular endothelial cells, might play a protective role in this procedure by inhibiting microvascular pericyte transformation and vascular loss. Abbreviations: PDGFR: platelet-derived growth factor receptor; TGFβ: transforming growth factor β; A1AR: A1 adenosine receptor.

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