Disrupting atherosclerosis

A team of German and U.S. researchers has designed a peptide that decreases atherosclerotic lesions in mice by disrupting interactions between two platelet-derived chemokines.1 The findings have led to the formation of Carolus Therapeutics Inc., which is developing the peptide for cardiovascular and inflammatory disorders.

Atherosclerotic lesions and plaques occur as a result of a series of inflammatory processes on the walls of blood vessels.2 In particular, adhesion of circulating leukocytes and platelets to inflamed arterial endothelial cells increases vessel permeability to plasma lipid components like plaque-forming low-density lipoprotein (LDL).

Over time, plaques accumulate, causing a narrowing of the vessel lumen. Occasionally, plaques rupture and release debris, triggering the formation of a thrombus, which canobstruct blood flow and result in myocardial infarction or stroke (see Figure 1, "Targeting chemokines in cardiovascular disease").

Marketed atherosclerosis drugs, like statins, target plasma lipids and are thought to trigger anti-inflammatory effects via mechanisms that are not fully elucidated.

Recently, researchers

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