The flagellin-TLR5-Nox4 axis promotes the migration of smooth muscle cells in atherosclerosis

Abstract

Atherosclerosis: halting plaque in its tracks TLR5-Nox4 signaling cascade plays a key role in atherosclerosis, hardening of the arteries, in which fatty deposits known as plaques accumulate in the inner walls of arteries. During plaque formation, vascular smooth muscle cells (VSMCs) migrate to the area and then collect fat molecules. The thickening plaques restrict blood flow. Inflammation was known to play a role in this process, but the activities of individual inflammatory molecules remained poorly understood. Yun Soo Bae at Ewha Womans University, Seoul, South Korea, and coworkers investigated how Nox4 affects plaque generation. They found that flagellin-TLR-5-Nox4 axis triggered VSMCs, leading to migrate and form an atherosclerotic plaque. In mice lacking Nox4, both VSMC migration and plaque formation were greatly reduced. These results may help in finding better treatments for this common cause of stroke and heart attack.