Role of Homocysteine in Endothelial Dysfunction During Experimental Atherosclerosis and Its Pharmacological Modulation

Endothelial dysfunction is a fundamental mechanism underlying the development of atherosclerosis and its complications. Among modifiable risk factors, hyperhomocysteinemia has emerged as a significant contributor to vascular injury. This study aimed to evaluate serum homocysteine levels in experimental atherosclerosis and to analyze their relationship with lipid metabolism and endothelial dysfunction. Hypercholesterolemia was induced in rabbits, followed by pharmacological correction using gemfibrozil, chitosan derivatives, and heparin. A progressive increase in homocysteine levels was observed during the development of atherosclerosis, accompanied by dyslipidemia and oxidative stress. Pharmacological interventions reduced homocysteine concentrations, with chitosan derivatives demonstrating the highest efficacy. The findings confirm the critical role of homocysteine in atherogenesis and highlight the therapeutic potential of chitosan-based compounds.

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