ARTICLE | Targets & Mechanisms

Blocking Blood Vessel Buildup

August 14, 2008 7:00 AM UTC

A study by Japanese and Austrian researchers published in The Journal of Clinical Investigation has uncovered a connection between the angiotensin II type 1 receptor and the lipoprotein receptor sortilin-related receptor, L(DLR class) A repeats-containing (LR11; SORL1) in vascular smooth muscle cells, suggesting that LR11 could be a better target for slowing or preventing vessel wall thickening and remodeling.1 According to researchers and companies polled by SciBX, although these findings may have some implications for atherosclerotic disease, more immediate benefits of targeting LR11 may lie in conditions caused by aberrant migration and proliferation of vascular smooth muscle cells, such as restenosis.

Vascular smooth muscle cells (VSMCs) line the walls of blood vessels and are responsible for changing local blood pressure by contracting or relaxing in response to neural and hormonal signals. During vascular injury, VSMCs migrate from the outer layers of a blood vessel (the media) to the innermost layer (the intima), which makes direct contact with flowing blood. There, VSMCs can contribute to remodeling and thickening of the vessel wall and, over time, can cause narrowing of the vessel lumen and restriction of local circulation.2,3...