Does Serum carboxymethyl lysine cause atherosclerosis?
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The Role of Serum Carboxymethyl Lysine in Atherosclerosis
Introduction to Carboxymethyl Lysine and Atherosclerosis
Carboxymethyl lysine (CML) is a prominent advanced glycation end product (AGE) that has been extensively studied for its role in various diseases, including diabetes and cardiovascular conditions. Atherosclerosis, a leading cause of morbidity and mortality worldwide, is characterized by the buildup of plaques in the arterial walls. This article explores the relationship between serum CML and the development of atherosclerosis.
CML and Its Presence in Arterial Walls
Research has shown that CML is significantly present in the arterial walls, particularly in the endothelial cells and intima of the arteries. This presence is more pronounced in older individuals, correlating with the progression of atherosclerosis. The accumulation of CML in the arterial walls is indicative of its role in the pathogenesis of atherosclerosis.
CML and Coronary Artery Disease
Studies have demonstrated that individuals with coronary artery disease (CAD) exhibit higher serum levels of CML compared to healthy individuals. This elevation is observed in both diabetic and non-diabetic patients with CAD, suggesting that CML is a potential biomarker for atherosclerosis irrespective of diabetic status . The increased serum CML levels in CAD patients highlight its association with the disease's severity and progression.
Mechanisms of CML-Induced Atherosclerosis
CML contributes to atherosclerosis through several mechanisms. One significant pathway involves the modification of low-density lipoprotein (LDL) particles. CML-modified LDL is less efficiently cleared from the bloodstream, leading to its accumulation and uptake by scavenger receptors on macrophages and vascular smooth muscle cells (SMCs). This process promotes the formation of foam cells, a hallmark of atherosclerotic plaques . Additionally, CML-induced foam cell apoptosis and vascular calcification further exacerbate atherosclerosis .
Oxidative Stress and CML
Oxidative stress plays a crucial role in the formation of CML. The imbalance between oxidative stress and antioxidants is a significant risk factor for atherosclerosis. Studies have shown that oxidative conditions accelerate the formation of CML, which in turn contributes to the oxidative damage observed in atherosclerotic lesions . The presence of CML in atherosclerotic plaques and its correlation with oxidative stress markers underscore its role in the disease's pathogenesis.
Dietary Influence on Serum CML Levels
Dietary intake is a major source of exposure to AGEs, including CML. However, studies have found that the consumption of foods high in CML does not significantly correlate with serum or urinary CML levels. This suggests that other factors, such as metabolic processes and individual variations, play a more critical role in determining serum CML levels.
Conclusion
In summary, serum carboxymethyl lysine (CML) is closely linked to the development and progression of atherosclerosis. Its presence in arterial walls, association with coronary artery disease, and involvement in oxidative stress and foam cell formation highlight its significance as a biomarker and potential therapeutic target. Understanding the mechanisms by which CML contributes to atherosclerosis can pave the way for better diagnostic and treatment strategies for cardiovascular diseases.
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