Targeting adenosine signaling to treatment of diabetic nephropathy.

摘要: Diabetic nephropathy (DN) continues being the primary cause of chronic hemodialysis and terminal renal disease worldwide. At tissue levels DN occurs with glomerulopathy affecting integrity filtration barrier an extensive glomerular tubule-interstitial fibrosis. Current available therapeutic approaches have only demonstrated a modest effect on progression kidney injury. Therefore, more research concerning pathomechanisms possible interventions are needed. Interestingly, in last years it has been documented that progresses growing nucleoside adenosine. This finding increased interest events controlling extracellular nucleoside. While metabolism ATP cyclic AMP well recognized sources, evidences regarding role equilibrative transporters adenosine availability promoting diabetic recently acquired pivotal role. The physiological effects mediated by P1 family receptors. It shown vivo use antagonist A2B receptor subtype can block most remarkable early alterations seen glomerulopathy. Furthermore, using models injury was fibrosis also be blocked treatment subtype. review highlights these findings correlate activity low affinity increase ligand pathological state. In addition, we discuss signaling regards to treatment.