12:00 AM
 | 
Jul 30, 2015
 |  BC Innovations  |  Targets & Mechanisms

Muscling in on atherosclerosis

Why targeting standard macrophages misses the mark in atherosclerosis

A finding from the University of Virginia overturning assumptions about the biology of atherosclerotic plaques could prompt companies to rethink their therapeutic strategies for the disease. Using a series of in vitro and in vivo studies, the team showed that about one third of the cells in plaques are of smooth muscle rather than immune cell origin, and proposed that going after the pathology of the smooth muscle cells could provide a new class of therapies to prevent heart attacks and stroke.

The dogma in the field has long been that atherosclerotic plaques have many more macrophages and monocyte-derived cells than smooth muscle cells, and companies have approached atherosclerosis as a chronic inflammatory disease.

The focus has been on targeting macrophages that accumulate in plaques and secrete inflammatory cytokines, because that process is thought to drive the plaque instability behind thrombotic events such as deep vein thrombosis (DVT) or pulmonary embolism.

But according to Gary Owens, lead investigator on the study, the dogma is based on faulty experimental methods that underestimate the contribution of smooth muscle cells to plaque formation.

"The evidence is based on use of methods that are unreliable in identifying which cells within the plaque are truly derived from macrophages versus smooth muscle cells, and even more importantly, what mechanisms regulate phenotypic transitions of these cells that are critical in the pathogenesis of the disease," he told BioCentury.

Owens is professor of cardiovascular research, molecular physiology and biological physics...

Read the full 1205 word article

User Sign in

Trial Subscription

Get a 4-week free trial subscription to BioCentury Innovations

Article Purchase

$100 USD
More Info >