Homocysteine Attack on Vascular Endothelium—Old and New Features
Abstract
Homocysteine (Hcy) is becoming a well-established risk factor for cardiovascular disease (CVD), mainly involving endothelial dysfunction and atherogenesis. Endothelial dysfunction is reflected primarily in the complex regulation of the main physiological and pathophysiological processes. There is increasing evidence regarding abnormally high concentrations of plasma total homocysteine, or plasma hyperhomocysteinemia, contributing to endothelial dysfunction, inflammation, and CVD. This clinical and experimental study examined the connection between Hcy and cardiovascular disease risk. Homocysteine is a marker of total vascular damage that must be monitored and controlled as early as possible. Dietary and lifestyle changes are recommended for most patients with hyperhomocysteinemia (Hhcy). The purpose of this paper is to review the data from the specialized literature that demonstrate that there is a direct link between endothelial injury and increased homocysteine levels, identifying existing evidence, describing new mechanisms, and exploring potential new therapeutic options. These aspects continue to be debated, and additional efforts are required to refine therapeutic strategies and to investigate the potential implications of Hcy in health and disease.
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