Department of Biochemistry and Molecular Biology in Disease, Nagasaki University Graduate School of Biomedical Sciences, Japan.
J Atheroscler Thromb. 2009 Oct;16(5):532-8. doi: 10.5551/jat.1255. Epub 2009 Sep 14.
Oxidative stress is believed to be a cause of aging and cardiovascular disorders. In response to inflam-mation or endothelial cell injury, production of reactive oxygen species (ROS) is enhanced in vascular cells. These changes contribute to the initiation of atherosclerosis. Vascular cells possess anti-oxidant systems to protect against oxidative stress, in addition to the redox system. The redox status of pro-tein thiols is important for cellular functions. The Akt signaling pathway exerts effects on survival and apoptosis, and is regulated by the glutathione (GSH)/glutaredoxin (GRX)-dependent redox sys-tem. Sex hormones such as estrogens protect against oxidative stress by protecting the Akt signaling pathway but the physiological role of the extracellular GSH/GRX system has not been clarified, although found an increase in the levels of S-glutathionylated serum proteins in patients with athero-sclerosis obliterans. The results suggested that impaired serum redox potential is a marker of the development vascular dysfunction and estrogen has a possible role in the prevention of atherosclerosis.
氧化应激被认为是衰老和心血管疾病的一个原因。在炎症或内皮细胞损伤的情况下，血管细胞中活性氧（ROS）的产生增加。这些变化导致动脉粥样硬化的发生。血管细胞除了具有氧化还原系统外，还具有抗氧化系统来防止氧化应激。蛋白质巯基的氧化还原状态对细胞功能很重要。Akt 信号通路对生存和凋亡有影响，并受谷胱甘肽（GSH）/谷胱甘肽还原酶（GRX）依赖性氧化还原系统的调节。雌激素等性激素通过保护 Akt 信号通路来抵抗氧化应激，但细胞外 GSH/GRX 系统的生理作用尚不清楚，尽管在闭塞性动脉硬化症患者的血清蛋白 S-谷胱甘肽化水平升高。结果表明，受损的血清氧化还原电势是血管功能障碍发展的标志物，雌激素可能在预防动脉粥样硬化方面发挥作用。
