Homocysteine: From an Emerging Biomarker to a Functional Indicator of Endothelial Dysfunction
Keywords:
Homocysteine, Endothelial Dysfunction, Cardiovascular Risk, Oxidative Stress, Cardiometabolic Prevention, NutraceuticalsAbstract
Homocysteine has emerged over recent decades as a significant biomarker associated with cardiovascular and cardiometabolic risk. Elevated plasma homocysteine levels have been linked to endothelial dysfunction, oxidative stress, inflammation, and prothrombotic states, all of which play a central role in the development and progression of atherosclerotic disease. This article provides an updated overview of the biological mechanisms through which homocysteine contributes to vascular damage, with particular attention to its impact on endothelial homeostasis.
The paper reviews current evidence on homocysteine metabolism, genetic and nutritional determinants of hyperhomocysteinemia, and its clinical relevance as a functional indicator rather than a mere biochemical marker. Special emphasis is placed on the interaction between homocysteine and B-group vitamins, oxidative pathways, and nitric oxide bioavailability, highlighting the multifactorial nature of endothelial impairment.
In addition, the role of targeted nutritional strategies and cardiovascular nutraceuticals in the management of elevated homocysteine levels is discussed, with reference to their potential contribution to primary and secondary prevention of cardiovascular disease. Rather than presenting new experimental data, this article aims to integrate existing clinical and pathophysiological knowledge to support a more comprehensive interpretation of homocysteine in cardiovascular risk assessment.
Overall, homocysteine is proposed as a clinically relevant functional indicator of endothelial dysfunction, offering useful insights for personalized prevention strategies in cardiometabolic medicine.
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