Molecular Research on Adenosine Receptors: From Cell Biology to Human Diseases
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 20 February 2025 | Viewed by 5385
Special Issue Editor
Interests: pharmacology; natural products; oxidative stress; inflammatory disease; atherosclerosis; metabolic disease; neurodegenerative diseases; autophagy; proliferation and differentiation process
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Adenosine is a ubiquitous endogenous cell signaling and modulator agent that plays a key role in the regulation of many physiological cell-signaling pathways; this nucleoside triggers a cellular response, activating four G-protein-coupled receptors (GPCRs) named the A1, A2A, A2B and A3 adenosine receptors (ARs). ARs are expressed in several tissues and organs, such as the brain, heart, bones, eyes, kidneys, skin, adipose tissue, immune cells, lungs and liver; due to their body distribution, ARs are implicated in several human disease, such as neurodegenerative disorders, chronic inflammatory diseases, cancer, hypoxia and ischemia. In many pathophysiological conditions, adenosine acts as a sensor for tissue damage, binding several AR-activating signaling pathways for the protection of damaged tissues or organs. Therefore, ARs could be considered a promising therapeutic target.
The purpose of this Special Issue of the International Journal of Molecular Sciences, entitled “Molecular Research on Adenosine Receptors: From Cell Biology to Human Diseases”, is to include original research papers and/or relevant literature data updates on novel insights into the pathogenesis, molecular pathways and beneficial effects of novel and safe AR agonist treatments.
Dr. Federica Mannino
Guest Editor
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Keywords
- adenosine
- ARs
- AR agonists
- chronic diseases
- therapeutic strategy
- AR antagonists
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