Adenosine metabolism

“Adenosine metabolism” refers collectively to all biochemical processes involving the synthesis and degradation of the purinergic nucleoside adenosine, including its conversion from ATP via enzymatic steps involving cytoplasmic/nuclear kinases and phosphatases such as ADK and NT5E/CD73. The process also includes its catabolism by ADA into inosines. These pathways regulate both intracellular energy homeostasis and extracellular signaling via four G protein-coupled receptor subtypes on various cell types throughout the body. Dysregulation contributes to pathologies ranging from cancer immunoevasion through local immunoinhibition, cardiovascular arrhythmias, neurodegeneration, inflammation, psychiatric disorders, and rare genetic diseases such as severe combined immunodeficiency due to ADA deficiency. In summary: “Adenosine metabolism” should not be used as an entry for an individual drug target, but instead broken down into its constituent enzymes/receptors/transporter proteins for structured data purposes. Each has unique biological roles—and many are validated therapeutic targets across diverse indications. If you need information on any specific enzyme/receptor within this pathway—for example “CD73,” “adenosinereceptor A₂ₐ,” or “adenosinedeaminase”—please specify so I can provide precise structured details about that entity.

Other names

Purinergic signaling pathwayAdenosinergic systemAdenosine metabolic pathway

Varies by component targeted: Agonism or antagonism at specific adenosinergic GPCRs modulates cAMP levels/signaling pathways affecting heart rate/rhythm or immune cell function. Inhibition of ecto-nucleotidases like CD39/CD73 reduces extracellular immunoregulatory/pro-tumorigenic effects by lowering local adenosine concentrations. Inhibition/blockade of nucleoside transporters alters intra/extracellular balance.