Abstract
Atherosclerosis is a complex process that involves the interaction between oxidized low-density lipoprotein (oxLDL) and macrophage. It is an inflammatory disease of the large artery driven by macrophage activation and infiltration. Through scavenger receptors, macrophages can uptake oxLDL and other lipids, leading to foam cell formation and the progression of atherosclerosis. Hv1 proton channel is highly expressed in phagocytes and promotes NADPH oxidase-derived ROS (reactive oxygen species) production. So far, most of the research on Hv1 has been focused on immune, reproductive, and neurological diseases. However, the role of Hv1 in cardiovascular diseases, such as arteriosclerosis, remains unclear. To explore the potential roles of Hv1 in atherosclerosis, we detected the expression of Hv1 in atherosclerotic lesions. It was shown that Hv1 is abundantly expressed in human and murine atherosclerotic lesions and highly expressed in macrophages in the aortic root lesions. In addition, Hv1 knockout mice fed with a high-fat western diet exhibit remarkably decreased atherosclerotic plaques compared with control mice. Moreover, deficiency of Hv1 in macrophages impedes macrophage phagocytosis and foam cell formation essential for atherosclerosis development, and Hv1 enhances macrophage ROS production associated with the progression of atherosclerosis. Our results suggested that Hv1 is a pro-atherosclerotic factor and contributes to the pathogenesis of atherosclerosis. The research identified a new function of the Hv1 channel in human diseases and may present a novel target against atherosclerosis and atherosclerosis-related diseases.
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