Editorial: Purinergic signaling in metabolic diseases and inflammation pharmacology

Numerous diseases, including obesity, diabetes, cardiovascular disorders, dementia-associated cognitive decline and sarcopenia are characterized by underlying inflammatory processes that contribute to disease progression. Purinergic signalling is widely recognized as a key modulator of inflammation. This system involves extracellular nucleotides (i.e., ATP, ADP, UTP, and UDP) and nucleosides (i.e., adenosine), which are detected by two receptor families: P2 receptors (for nucleotides) and P1 receptors (for nucleosides), expressed on various cell types. The regulation of extracellular ATP and adenosine levels is mediated by ecto-enzymes, particularly NTPDase1/CD39 and 5′-Nucleotidase/CD73, which sequentially degrade ATP to adenosine, as well as by nucleotide/nucleoside transporters. Generally, ATP-activated P2 receptors promote pro-inflammatory responses, whereas adenosine, acting via P1 receptors, exerts predominantly anti-inflammatory and immunosuppressive effects. Consequently, modulating inflammatory conditions through purinergic signalling may represent a promising therapeutic strategy for these diseases. In this Research Topic we have compiled six original research articles that provide up-to-date insights into the role of purinergic signalling in different inflammatory diseases.