Hypertension, obesity, diabetes, atherosclerosis, cardiovascular diseases, cancer, among others, are common pathologic conditions, especially in elderly. These diseases show various interrelations, and they all share the important role of inflammation in the initiation and/or progression of disease. Furthermore, systemic inflammation plays an essential role in the development of metabolic diseases. Purinergic signaling is recognized as a major player in inflammation. It consists of extracellular nucleotides (i.e., ATP, ADP, UTP, and UDP) and nucleosides (i.e., adenosine), which are recognized by two families of receptors, P2 receptors for nucleotides and P1 receptors for nucleosides, expressed on different cell types. In addition, several ecto-enzymes, especially NTPDase1/CD39 and NT5E/CD73, are responsible of the conversion of extracellular ATP to the final product adenosine. Extracellular ATP, acting on P2 receptors, exerts a pro-inflammatory activity, while adenosine, through the P1 receptors, acts mainly as an anti-inflammatory and immunosuppressive agent. Therefore, purinergic signaling represents a comprehensive system able to regulate inflammation.
Inflammatory and metabolic disorders are in great expansion. Therefore, the role of purinergic signaling in this field deserves further exploration to focus on new pathogenetic aspects and possible targets of latest pharmacological therapies.
This Research Topic aims to publish high-quality scholarly papers in relation to all critical aspects of inflammation, including the identification of drugs for inflammation-related diseases as well biomarkers of drug efficacy and toxicity. It aims to highlight recent advances in the field, whilst emphasizing important directions and new possibilities for future inquiries. We anticipate the articles presented will promote discussion in the scientific community that will translate to best practice applications in clinical, public health and policy settings. This exciting collection welcomes original research, full-length, mini or systematic review papers.
Hypertension, obesity, diabetes, atherosclerosis, cardiovascular diseases, cancer, among others, are common pathologic conditions, especially in elderly. These diseases show various interrelations, and they all share the important role of inflammation in the initiation and/or progression of disease. Furthermore, systemic inflammation plays an essential role in the development of metabolic diseases. Purinergic signaling is recognized as a major player in inflammation. It consists of extracellular nucleotides (i.e., ATP, ADP, UTP, and UDP) and nucleosides (i.e., adenosine), which are recognized by two families of receptors, P2 receptors for nucleotides and P1 receptors for nucleosides, expressed on different cell types. In addition, several ecto-enzymes, especially NTPDase1/CD39 and NT5E/CD73, are responsible of the conversion of extracellular ATP to the final product adenosine. Extracellular ATP, acting on P2 receptors, exerts a pro-inflammatory activity, while adenosine, through the P1 receptors, acts mainly as an anti-inflammatory and immunosuppressive agent. Therefore, purinergic signaling represents a comprehensive system able to regulate inflammation.
Inflammatory and metabolic disorders are in great expansion. Therefore, the role of purinergic signaling in this field deserves further exploration to focus on new pathogenetic aspects and possible targets of latest pharmacological therapies.
This Research Topic aims to publish high-quality scholarly papers in relation to all critical aspects of inflammation, including the identification of drugs for inflammation-related diseases as well biomarkers of drug efficacy and toxicity. It aims to highlight recent advances in the field, whilst emphasizing important directions and new possibilities for future inquiries. We anticipate the articles presented will promote discussion in the scientific community that will translate to best practice applications in clinical, public health and policy settings. This exciting collection welcomes original research, full-length, mini or systematic review papers.