4.7 Review

Potential for modulation of platelet function via adenosine receptors during inflammation

Journal

BRITISH JOURNAL OF PHARMACOLOGY
Volume -, Issue -, Pages -

Publisher

WILEY
DOI: 10.1111/bph.16146

Keywords

adenosine; adenosine receptors; blood platelet; immune system; immunity; inflammation

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Traditionally, platelets are known for their role in haemostasis and thrombosis, but they also play a crucial role in inflammation and immunity. Platelets secrete molecules and interact with cells, and they express receptors involved in pathogen recognition. Platelet adenosine receptors, specifically the A(2A) and A(2B) subtypes, have been identified as potential targets for inhibiting platelet activation and down-regulating inflammation or immunity. This article reviews the pharmacological potential of adenosine and other agonists of these receptors in modulating platelet function during inflammation.
Traditionally, platelets are known to play an important role in haemostasis and thrombosis; however, they serve also as important modulators of inflammation and immunity. Platelets secrete adhesion molecules and cytokines, interact with leukocytes and endothelium, and express toll-like receptors involved in a direct interaction with pathogens. Platelets express A(2A) and A(2B) subtypes of receptors for adenosine. The activation of these receptors leads to an increase in cAMP concentration in the cytoplasm, thereby resulting in inhibited secretion of pro-inflammatory mediators and reduced cell activation. Therefore, platelet adenosine receptors could be a potential target for inhibiting platelet activation and thus down-regulating inflammation or immunity. The biological effects of adenosine are short-lasting, because the compound is rapidly metabolized; hence, its lability has triggered efforts to synthesize new, longer-lasting adenosine analogues. In this article, we have reviewed the literature regarding the pharmacological potential of adenosine and other agonists of A(2A) and A(2B) receptors to affect platelet function during inflammation.

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