Atherosclerosis underlies most heart attacks and strokes and is now recognized as a chronic inflammatory disease rather than a simple disorder of cholesterol deposition. While immune cells such as macrophages have been widely studied, emerging evidence shows that vascular smooth muscle cells also play a central role in plaque development. These cells exhibit remarkable plasticity, contributing either to plaque stabilization or to inflammation and tissue breakdown. However, the molecular signals that determine whether smooth muscle cells adopt protective or pathogenic identities have remained poorly defined. Based on these challenges, there is a critical need to identify the regulatory mechanisms that drive harmful smooth muscle cell phenotype switching and promote plaque instability.
Researchers from the…