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The prostacyclin pathway centers on the endogenous molecule prostacyclin (PGI2), primarily synthesized by vascular endothelial cells. It plays a critical role in cardiovascular homeostasis, especially in regulating vascular tone, inhibiting platelet aggregation, and suppressing smooth muscle cell proliferation. It achieves these effects via activation of the IP receptor and downstream signaling cascades. Reduced PGI2 production is implicated in pulmonary arterial hypertension, making this pathway a target for therapeutic intervention.
Prostacyclin and its analogs activate the IP receptor, a G protein-coupled receptor, leading to increased intracellular cAMP levels, activation of protein kinase A (PKA) and exchange proteins activated by cAMP (Epac), resulting in vasodilation and inhibition of platelet aggregation.
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