高同型半胱氨酸血症导致动脉粥样硬化氧化应激机制的研究进展

Research Progress of Oxidative Stress Mechanisms of High Hyperhomocysteinemia Causing Atherosclerosis

同型半胱氨酸(Hcy)是一种含硫氨基酸,它可通过多种途径介导动脉粥样硬化,其促进动脉粥样硬化形成的机制,包括氧化应激、炎性反应、内皮功能障碍、血管平滑肌细胞增殖、内质网应激等,血管细胞氧化应激被认为是导致血管损伤的重要机制之一。Hcy通过诱导活性氧类自由基产生增加,改变许多细胞的分子结构,导致细胞功能受损,进而导致动脉粥样硬化。

Homocysteine is a type of sulfur-containing amino acids. Several hypotheses have been pro- posed to explain the cellular mechanisms of high hyperhomocysteinemia promoting atherosclerosis, including oxidative stress, inflammatory response, endothelial dysfunction, vascular smooth muscle cell proliferation, reticulum stress. Vascular cell oxidative stress is considered to be one of the important mechanisms that cause vascular injuries. Homocysteine increases production of the reactive oxygen species （ ROS ） , changing the molecular structure of many cells, resulting in impaired cell function, and leading to atherosclerosis.