TRPV1: a useful therapeutic target for patients with vulnerable coronary plaques

Acute coronary syndromes are generally caused by atherosclerotic plaque rupture. Inflammation is one of the most important features of vulnerable plaque. Adventitial vanilloid receptor TRPV1 and sensory C-fibers may play a pistol role for adventitial inflammation. TRPV1 is also present in platelets, and the presence of this receptor may provide a link between inflammatory mediators and platelet activation in atherosclerosis. The hypothesis we propose here is that TRPV1 may be a useful therapeutic target for patients with vulnerable coronary plaques. The fact that statins act directly on sensory neurons to decrease expression of proinflammatory neuropeptides, supports our hypothesis as above. However, the mechanisms mediating this potential effect are poorly understood. Future studies are required to determine whether downregulated expression of TRPV1 contributes to these therapeutic actions.