Adenosine, a ubiquitous endogenous autacoid, acts through the enrollment of four G protein-coupled receptors: A1, A2A, A2B, and A3. Adenosine affects almost all aspects of cellular physiology, including neuronal activity, vascular function, platelet aggregation, and blood cell regulation[1]. Adenosine is formed by enzymatic degradation of adenosine triphosphate and eliminated by phosphorylation to adenosine monophosphate or by deamination to inosine. Extracellular adenosine as a signaling molecule binds to adenosine receptors, which may trigger via their cognate trimeric G proteins different signaling pathways[2]. As the core molecule of adenosine triphosphate (ATP), adenosine exists in equilibrium with the adenine nucleotide pool and contributes to cellular energy charge, a quantification of relative amounts of available ATP, ADP, AMP and adenosine. Beyond participating in overall energy balance and thus in maintaining cellular homeostasis, adenosine critically influences dynamic signaling in the nervous system. In particular, adenosine has an effect on and is affected by excitatory synaptic transmission[3]. Adenosine is a common metabolite of ATP, which exhibits cytotoxic effects at high concentrations. Adenosine (1.0-4.0 mM; 12-24 hours) inhibits cell viability and triggers ER stress in HepG2 cells. Adenosine (2.0 mM; 12-24 hours) induces autophagy in HepG2 cells [4].
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