A(2A) adenosine receptor: a novel therapeutic target in renal disease

Present strategies in the treatment of inflammatory renal injury have focused on developing agents that specifically target individual mechanisms thought to contribute toward the pathogenesis of the disease. Such an approach is hindered by redundancies in the inflammatory cascade, rendering intervention suboptimal. The A(2A) adenosine receptor (A(2A)-AR) is a member of the family of guanine nucleotide binding proteins and has become a focus of major interest primarily because of its ability to broadly inactivate the inflammatory cascade. This review summarizes our present knowledge regarding the molecular biology and pharmacology of A(2A)-ARs as well as the physiological effects of activation of A(2A)-ARs in the kidney. We also review our recent experience in targeting this receptor subtype in abrogating the inflammatory cascade in ischemia-reperfusion injury.