Understanding Atherosclerosis: The Role of LDL and Oxidative Stress

The formation of atherosclerotic plaques involves complex interactions at the cellular level, primarily driven by the entry of lipoproteins, produced by the liver, into the vascular endothelium. While these lipoproteins deliver essential fat-soluble nutrients like vitamins D, K, and coenzyme Q10 without causing plaque, certain conditions can lead to their retention and trigger atherosclerosis. The accumulation of modified LDL lipoprotein can initiate a cascade involving macrophages, leading to foam cell formation and plaque. The key insight lies in understanding the unique variables and conditions, such as increased oxidative stress, that predispose some individuals to greater plaque formation despite the necessity of LDL for cellular functions.