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[Less common risk factors for atherogenesis--homocysteine, lipoprotein (a) and C-reactive protein]
1Ustav klinické biochemie a laboratorní diagnostiky LF UK a FN, Plzen. racek@fnplzen.cz
Insights
Atherosclerosis risk extends beyond traditional factors. Homocysteine, lipoprotein (a), and C-reactive protein significantly contribute to endothelial dysfunction, a key early stage of atherogenesis.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Pathophysiology
Context:
- Atherosclerosis is a leading cause of death globally.
- Classical risk factors like hypertension and hypercholesterolemia do not explain all early atherosclerosis cases.
Purpose:
- To review emerging risk factors for atherosclerosis.
- To explore the roles of homocysteine, lipoprotein (a), and highly sensitive C-reactive protein.
- To examine their metabolic links and impact on endothelial dysfunction.
Summary:
- This review highlights homocysteine, lipoprotein (a), and highly sensitive C-reactive protein as significant contributors to atherosclerosis.
- These factors, though distinct, converge in promoting endothelial dysfunction, the initial phase of atherogenesis.
- Understanding these risks offers new avenues for intervention.
Impact:
- Identifies key non-classical risk factors for cardiovascular disease.
- Emphasizes endothelial dysfunction as a critical early mechanism.
- Provides insights for developing novel diagnostic and therapeutic strategies.
Abstract:
Atherosclerosis and its complications belong to the most frequent causes of morbidity and mortality in the developed countries. Far from all cases of early atherosclerosis can be explained by presence of "classical" risk factors (hypertension, hypercholesterolemia, and namely by oxidised forms of lipoproteins of low density, by smoking or due to not fully compensated diabetes mellitus). Our review brings information of another three serious risk factors--homocysteine, lipoprotein (a), and highly sensitive C-reactive protein. Metabolic relations among them are given as well as results of comparatively independent clinical studies and possibilities to influence these risk factors. Though they are comparatively independent, one feature connects them--they participate significantly on the development of endothelial dysfunction, which is supposed to be the initial stadium of atherogenesis.