The cell origins of foam cell and lipid metabolism regulated by mechanical stress in atherosclerosis

Atherosclerosis is an inflammatory disease initiated by endothelial activation, in which lipoprotein, cholesterol, extracellular matrix, and various types of immune and non-immune cells are accumulated and formed into plaques on the arterial wall suffering from disturbed flow, characterized by low and oscillating shear stress. Foam cells are a major cellular component in atherosclerotic plaques, which play an indispensable role in the occurrence, development and rupture of atherosclerotic plaques. It was previously believed that foam cells were derived from macrophages or smooth muscle cells, but recent studies have suggested that there are other sources of foam cells. Many studies have found that the distribution of atherosclerotic plaques is not random but distributed at the bend and bifurcation of the arterial tree. The development and rupture of atherosclerotic plaque are affected by mechanical stress. In this review, we reviewed the advances in foam cell formation in atherosclerosis and the regulation of atherosclerotic plaque and lipid metabolism by mechanical forces. These findings provide new clues for investigating the mechanisms of atherosclerotic plaque formation and progression.

Automated summary

Atherosclerosis is an inflammatory disease initiated by endothelial activation, in which various components like lipoprotein, cholesterol, extracellular matrix, and immune and non-immune cells accumulate and form plaques on the arterial wall. Foam cells, previously believed to be derived from macrophages or smooth muscle cells, play a crucial role in the occurrence, development, and rupture of atherosclerotic plaques. The distribution of atherosclerotic plaques is not random, but concentrated at the bend and bifurcation of the arterial tree. Mechanical stress affects the development and rupture of atherosclerotic plaques, and this review discusses the advances in understanding foam cell formation, plaque regulation, and lipid metabolism regulation by mechanical forces in atherosclerosis.