Abstract

Atherosclerosis, a condition affecting the large arteries, stands as the leading cause of heart disease and stroke. In westernized societies, it accounts for approximately 50% of all deaths. While epidemiological studies have identified crucial environmental and genetic risk factors linked to atherosclerosis, its etiological complexity has impeded progress in understanding the underlying mechanisms. Fortunately, advancements in investigative tools over the past decade, such as genetically modified mouse models of the disease, have shed light on the molecular interactions involved. These insights have revealed the intricate connections between altered cholesterol metabolism, other risk factors, and the formation of atherosclerotic plaque. We now comprehend that atherosclerosis is not merely an inevitable consequence of aging but rather a chronic inflammatory condition. This condition can turn into an acute clinical event when plaque rupture and thrombosis occur. With this improved understanding, we are better equipped to address the complexities of atherosclerosis and potentially develop more effective treatments to combat its devastating consequences.