Key result
Purinergic receptors, specifically P2X4, P2X7, P2Y1, and P2Y12, mediate endothelial dysfunction by regulating vascular tone, inflammation, and platelet activity, serving as potential therapeutic targets for atherosclerosis.
This review highlights the mechanistic role of purinergic signaling in endothelial dysfunction, suggesting specific purinergic receptors as potential therapeutic targets for atherosclerosis.
Supports purinergic receptor targeting in atherosclerosis; leaves open clinical translation pending interventional trials.
Atherosclerosis is the main pathological basis of cardiovascular disease and involves damage to vascular endothelial cells (ECs) that results in endothelial dysfunction (ED). The vascular endothelium is the key to maintaining blood vessel health and homeostasis. ED is a complex pathological process involving inflammation, shear stress, vascular tone, adhesion of leukocytes to ECs, and platelet aggregation. The activation of P2X4, P2X7, and P2Y2 receptors regulates vascular tone in response to shear stress, while activation of the A2A, P2X4, P2X7, P2Y1, P2Y2, P2Y6, and P2Y12 receptors promotes the secretion of inflammatory cytokines. Finally, P2X1, P2Y1, and P2Y12 receptor activation regulates platelet activity. These purinergic receptors mediate ED and participate in atherosclerosis. In short, P2X4, P2X7, P2Y1, and P2Y12 receptors are potential therapeutic targets for atherosclerosis.
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Wu et al. (2022) conducted a review in Atherosclerosis and endothelial dysfunction. Purinergic receptors (P2X4, P2X7, P2Y1, P2Y12) was evaluated. Purinergic receptors, specifically P2X4, P2X7, P2Y1, and P2Y12, mediate endothelial dysfunction by regulating vascular tone, inflammation, and platelet activity, serving as potential therapeutic targets for atherosclerosis.
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