The role of monocytes/macrophages in the pathogenesis of ischemia-reperfusion injury (IRI)
is unknown. We sought to determine whether activation of macrophage adenosine 2A (A2A)�…

We sought to determine the mechanisms responsible for the reduced renal tissue injury by
agonists of A2A adenosine receptors (A2A-ARs) in models of ischemia-reperfusion (I/R)�…

Activation of A2A adenosine receptors (A2ARs) protects kidneys from ischemia-reperfusion
injury (IRI). A2ARs are expressed on bone marrow–derived (BM-derived) cells and renal�…

It was previously demonstrated that preischemic A 1 adenosine receptor (AR) activation
protects renal function after ischemia-reperfusion (IR) injury in rats. The role of the A 1 AR in�…

Abstract A 2A adenosine receptor (A 2A R)-expressing bone marrow (BM)-derived cells
contribute to the renal protective effect of A 2A agonists in renal ischemia-reperfusion injury�…

Enhanced protection from renal ischemia: Reperfusion injury with A 2A-adenosine receptor
activation and PDE 4 inhibition. Background We previously demonstrated in rats and mice�…

We showed previously that activation of A1 adenosine receptors (AR) protects against renal
ischemia-reperfusion (IR) injury in rats and mice. In the heart, transient A1AR activation�…

Controversy exists regarding the effect of A1 adenosine receptor (AR) activation in the
kidney during ischemia and reperfusion (I/R) injury. We sought to further characterize the�…

Genetic deletion of the adenosine A1 receptor (A1AR) increased renal injury following
ischemia–reperfusion injury suggesting that receptor activation is protective in vivo. Here we�…

A2A adenosine receptors (A2A-ARs) are known modulators of renal hemodynamics and
potent inhibitors of inflammation. We sought to determine whether selective activation of A2A�…