Alteration of purinergic signaling in diabetes: Focus on vascular function

摘要: Diabetes is an important risk factor for the development of cardiovascular disease including atherosclerosis and ischemic heart disease. Vascular complications macro- micro-vascular dysfunction are leading causes morbidity mortality in diabetes. Disease mechanisms at present unclear no ideal therapies available, which urgently calls identification novel therapeutic targets/agents. An altered nucleotide- nucleoside-mediated purinergic signaling has been implicated to cause diabetes-associated vascular major organs. Alteration both P1 P2 receptor sensitivity rather than changes expression accounts Activation P2X7 receptors plays a crucial role diabetes-induced retinal microvascular dysfunction. Recent findings have revealed that ecto-nucleotidase CD39, key enzyme hydrolyzing ATP, CD73, regulating adenosine turnover, involved renal injury Interestingly, erythrocyte diabetes by decreasing ATP release response physiological stimuli may serve as trigger induce Nucleot(s)ide-mediated activation also exerts long-term actions inflammatory atherogenic effects hyperglycemic diabetic conditions. This review highlights current knowledge regarding nucleot(s)ide-mediated mechanism complications. Better understanding receptor-mediated will provide more insights into their potential targets treatment.