ANGPTL4 stabilizes atherosclerotic plaques and modulates the phenotypic transition of vascular smooth muscle cells through KLF4 downregulation

Abstract

Cardiovascular disease: Stopping and stabilizing atherosclerotic plaques Treatment with a protein that stabilizes existing plaques within blood vessels could help reduce the risk of future cardiovascular events in patients with atherosclerosis. These plaques arise in part from a change in the behavior of the muscle cells within the walls of the blood vessels, which leads to the accumulation of lipids and other biomolecules and creates conditions that can ultimately result in a heart attack or stroke. Researchers led by Youngkeun Ahn and Yong Sook Kim at Chonnam National University Hospital, Gwangju, South Korea, have shown that they can counter this process in a mouse model of atherosclerosis by treatment with a protein called ANGPTL4. This molecule keeps vascular muscle cells in a state that prevents further plaque formation, while stabilizing existing plaques and countering the inflammatory processes that can further accelerate the cardiovascular disease.