1. Volume 86, Issue 4, Pages 685-692 (October 2014)
The role of adenosine receptors A2A and A2B signaling in renal fibrosis 
Veena S. Roberts, Peter J. Cowan, Stephen I. Alexander, Simon C. Robson, Karen M. Dwyer 
Kidney International 
Volume 86, Issue 4, Pages (October 2014)
DOI: /ki
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2. Figure 1 Extracellular purinergic catabolic and signaling pathways.
Kidney International  , DOI: ( /ki )
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3. Figure 2
Adenosine inhibits the expression of pro-inflammatory cytokines by M1 macrophages via A2AR signaling, and promotes a shift to the anti-inflammatory M2 phenotype via A2BR signaling.
Kidney International  , DOI: ( /ki )
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4. Figure 3
Adenosine signaling via A2AR and A2BR reduces inflammation. (Left panel) Renal injury promotes macrophage and T effector cell infiltration that is associated with increased inflammation and renal fibrosis. Cellular damage releases adenosine triphosphate (ATP), which is hydrolyzed to adenosine by extracellular CD39 and CD73. Equilibrative nucleoside transporter (ENT) removes adenosine from the extracellular space into the intracellular space and is distributed on the blood vessels and tubular cells. (Right panel) Adenosine signaling via A2AR and A2BR reduces infiltration of T-effector and M1 macrophages and promotes generation of regulatory T cells and M2 macrophages, which are associated with reduced inflammation and less fibrosis.
Kidney International  , DOI: ( /ki )
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5. Figure 4
Experimental models of hypertension and diabetes reveal increased adenosine generation and A2BR expression. A2BR activation on fibroblasts and mesangial cells promotes extracellular matrix deposition driving the development of renal fibrosis. Vasoconstriction mediated by endothelin-1 promotes hypoxia which is perpetuated by renal fibrosis. Chronic hypoxia further drives adenosine generation and A2BR activity, creating a vicious cycle of chronic hypoxia and renal fibrosis.
Kidney International  , DOI: ( /ki )
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