Strategies to identify and treat early atherosclerosis are urgently needed to reduce the risk of cardiovascular complications. A paper in Nature now reports that imidazole propionate (ImP), a molecule made by bacteria residing in the gut, contributes to atherosclerosis development in mice and is linked to early active atherosclerosis in humans. In mice, pharmacological blockade of the imidazoline-1 receptor (I1R), which is expressed in several cell types including myeloid cells, inhibited ImP- or high-cholesterol-induced atherosclerosis development.
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