What question did this study set out to answer?

To outline and discuss the biological and molecular mechanisms through which hyperhomocysteinemia promotes endothelial dysfunction in cardiovascular disease.

April 29, 2009Current Hypertension ReviewsOpen Access

Hyperhomocysteinemia and Endothelial Dysfunction

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Authors

ZCZhongjian ChengTemple College XYXiaofeng YangArmy Medical University HWHong WangNortheast Agricultural University

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Implication

Narrative review reveals mechanisms linking hyperhomocysteinemia to vascular endothelial dysfunction, indicating multiple pathways driving early cardiovascular pathology.

Key Points

To outline and discuss the biological and molecular mechanisms through which hyperhomocysteinemia promotes endothelial dysfunction in cardiovascular disease.
Reviewed cellular, animal, and human data evaluating vascular consequences of hyperhomocysteinemia.
Examined hyperhomocysteinemia experimental models driven by dietary high-methionine loading or genetic enzyme deficiencies.
Identified six primary pathways responsible for endothelial dysfunction: nitric oxide inhibition, prostanoid dysregulation, suppression of endothelium-derived hyperpolarizing factors, angiotensin II receptor-1 activation, endothelin-1 induction, and oxidative stress.
Established endothelial dysfunction as the primary early biomarker mediating elevated homocysteine-induced vascular injury and progression toward clinical atherosclerosis.

Cite This Study

Cheng et al. (2009) studied this question.

synapsesocial.com/papers/6a71954f6ceb2bbd16e02feb https://doi.org/10.2174/157340209788166940

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Implication

Narrative review reveals mechanisms linking hyperhomocysteinemia to vascular endothelial dysfunction, indicating multiple pathways driving early cardiovascular pathology.

Hyperhomocysteinemia and Endothelial Dysfunction

Discussion

Member takes

Implication

Key Points

Cite This Study

Hyperhomocysteinemia and Endothelial Dysfunction

Discussion

Member takes

Implication

Key Points

Cite This Study

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