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Updated: Aug 24, 2026

Measurement of Heme Synthesis Levels in Mammalian Cells
Published on: July 9, 2015
[Homocysteine: why is it harmful?]
1Laboratory for Clinical Problems of Atherosclerosis, A. L. Myasnikov Institute of Clinical Cardiology, Russian Scientific Cardiology Complex, RF Ministry of Public Health, Moscow, Russia.
Insights
Hyperhomocysteinemia damages blood vessels by negatively impacting vessel walls, cell interactions, and blood clotting. Understanding these mechanisms is crucial for preventing vascular disease.
Area of Science:
- Vascular Biology
- Biochemistry
- Pathophysiology
Context:
- Hyperhomocysteinemia is an established risk factor for vascular disease.
- The precise mechanisms linking homocysteine to vascular damage require detailed elucidation.
Purpose:
- To comprehensively review the pathogenetic mechanisms of hyperhomocysteinemia-induced vascular damage.
- To consolidate current understanding of how elevated homocysteine affects the vasculature.
Summary:
- Hyperhomocysteinemia adversely affects endothelial and smooth muscle cell function, impairing vessel wall integrity and vasodilatation.
- It promotes prothrombotic states by influencing coagulation factors and blood cell interactions like monocyte and platelet adhesion.
- Homocysteine also impacts vascular adenosine levels, further contributing to endothelial dysfunction.
Impact:
- Provides a foundational understanding for developing targeted therapies against hyperhomocysteinemia-related vascular complications.
- Highlights key molecular pathways involved in homocysteine-induced endothelial dysfunction and thrombosis.
- Informs clinical strategies for risk assessment and management of patients with elevated homocysteine levels.
Abstract:
This paper discusses the potential pathogenetic mechanisms by which the damaging action of hyperhomocysteinemia on the vessels is realized, namely a negative effect on the structure and function of the vessel wall, on proliferation of smooth muscle cells and endothelium-dependent vasodilatation; on the processes of blood cell interaction with the vessel wall (adhesion of monocytes, platelet adhesion and aggregation, etc): prothrombogenic action on the coagulation system, and effect of homocysteine on adenosine concentration in plasma and tissues.
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