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Updated: Jun 10, 2026

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Published on: June 10, 2025
Physiological implications of adenosine receptor-mediated platelet aggregation
Hillary A Johnston-Cox1, Dan Yang, Katya Ravid
1Departments of Medicine and Biochemistry, Whitaker Cardiovascular Institute, Evans Center for Interdisciplinary Biomedical Research, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Adenosine inhibits platelet activation by binding to A(2) receptors, increasing cyclic adenosine monophosphate (cAMP). This review highlights adenosine
Area of Science:
- Biochemistry and Molecular Biology
- Hematology
- Pharmacology
Background:
- Adenosine is a key metabolite involved in regulating platelet function.
- Platelet activation is a critical process in hemostasis and thrombosis.
- Adenosine exerts its effects through specific cell surface receptors.
Purpose of the Study:
- To review the role and significance of adenosine and its receptors in platelet physiology.
- To discuss the mechanisms by which adenosine inhibits platelet activation.
- To highlight recent findings on the A(2B) adenosine receptor's function in platelet modulation.
Main Methods:
- Literature review of scientific publications on adenosine, platelet activation, and adenosine receptors.
- Analysis of studies investigating the signaling pathways involving adenosine receptors and cyclic adenosine monophosphate (cAMP).
- Examination of research detailing the A(2B) adenosine receptor's influence on adenosine diphosphate (ADP) receptor expression.
Main Results:
- Adenosine binding to A(2A) and A(2B) adenosine receptors increases intracellular cAMP levels.
- Elevated cAMP is a potent inhibitor of platelet activation.
- The A(2B) adenosine receptor modulates platelet activation via control of ADP receptor expression.
Conclusions:
- Adenosine is a critical endogenous inhibitor of platelet activation.
- Adenosine receptors, particularly A(2B), play significant roles in platelet physiology and regulation.
- Understanding these interactions provides insights into potential therapeutic targets for thrombotic disorders.
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