Blocking a receptor called DP1 to prevent niacin (vitamin B3) flushing may increase susceptibility to aneurysms. (2012) Digest
From the article:
Niacin, or vitamin B3, is the one approved drug that elevates “good” cholesterol (high density lipoprotein, HDL) while depressing “bad” cholesterol (low density lipoprotein , LDL), and has thereby attracted much attention from patients and physicians. Niacin keeps fat from breaking down, and so obstructs the availability of LDL building blocks.
Patients often stop taking niacin because it causes uncomfortable facial flushing, an effect caused by the release of a fat called prostaglandin or (PG)D2. PGD2 is the primary cause of the unwanted vasodilation, the “niacin flush.” The dilation occurs when blood vessels widen from relaxed smooth muscle cells within vessel walls.
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PGD2, formed by an enzyme called COX-2 and released by immune and skin cells, acts on a muscle cell-surface receptor called DP1 to cause the flushing.
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However, deletion of DP1 made mice somewhat more susceptible to hardening of the arteries, the formation of aneurysm, thrombosis, and in some cases, high blood pressure. The researchers suggest that these findings are reflective of DP1 expression in vascular and immune cells in mice, just as in humans, despite its absence on mouse platelet cells.