Junjie Zhao1, Hailin Chen1, Ning Liu2, Jun Chen1, Youquan Gu1, Jiangjun Chen1, Kui Yang1. 1. Department of Neurology, Zhoukou Central Hospital, Zhoukou, Henan 466000, China. 2. Department of Neurology, Zhoukou Central Hospital, Zhoukou, Henan 466000, China. Electronic address: Lnning1957@sina.com.
Abstract
BACKGROUND: The mechanisms of hyperhomocysteinemia (HHcy) and hyperuricemia (HUA) that promote atherosclerosis were seldom explored and always indefinite. Therefore, we will discuss some new reviews about the role of HHcy and HUA in the pathogenesis of atherosclerosis. METHODS: This study was conducted by reading a lot of literature, including basic research and clinical application research. RESULTS: HHcy is known as an independent risk factor for atherosclerosis. Possible mechanisms for the association between homocysteine and atherosclerosis include stimulating smooth muscle cell growth, reducing endothelial cell growth and endothelial cell relaxation, and decreasing synthesis of high-density lipoprotein. HUA causes endothelial dysfunction and thereby increases oxidative stress, inducing vascular smooth muscle cell proliferation and reducing endothelial nitric oxide bioavailability. HUA plays a role in the development and pathogenesis of metabolic syndrome, hypertension, stroke, and atherosclerosis. CONCLUSIONS: Accelerated atherosclerosis may be a consequence of the combined effect of HHcy and HUA.
BACKGROUND: The mechanisms of hyperhomocysteinemia (HHcy) and hyperuricemia (HUA) that promote atherosclerosis were seldom explored and always indefinite. Therefore, we will discuss some new reviews about the role of HHcy and HUA in the pathogenesis of atherosclerosis. METHODS: This study was conducted by reading a lot of literature, including basic research and clinical application research. RESULTS: HHcy is known as an independent risk factor for atherosclerosis. Possible mechanisms for the association between homocysteine and atherosclerosis include stimulating smooth muscle cell growth, reducing endothelial cell growth and endothelial cell relaxation, and decreasing synthesis of high-density lipoprotein. HUA causes endothelial dysfunction and thereby increases oxidative stress, inducing vascular smooth muscle cell proliferation and reducing endothelial nitric oxide bioavailability. HUA plays a role in the development and pathogenesis of metabolic syndrome, hypertension, stroke, and atherosclerosis. CONCLUSIONS: Accelerated atherosclerosis may be a consequence of the combined effect of HHcy and HUA.
Authors: Andrea Sansone; Angelo Cignarelli; Massimiliano Sansone; Francesco Romanelli; Giovanni Corona; Daniele Gianfrilli; Andrea Isidori; Francesco Giorgino; Andrea Lenzi Journal: Int J Endocrinol Date: 2018-08-07 Impact factor: 3.257
Authors: Alan D Kaye; George M Jeha; Alex D Pham; Mitchell C Fuller; Zachary I Lerner; Gerald T Sibley; Elyse M Cornett; Ivan Urits; Omar Viswanath; Christopher G Kevil Journal: Adv Ther Date: 2020-08-26 Impact factor: 3.845