Inflammation plays a central role in the development of atherosclerosis, a condition characterized by the buildup of cholesterol and other substances in the arteries. Initially viewed as a cholesterol storage disease, atherosclerosis has been redefined through research showing that inflammation is a key driver of the disease. The discovery of immune mechanisms in atherosclerosis, such as the role of macrophages and inflammatory cells, has transformed understanding of the disease. Inflammation not only promotes plaque formation but also contributes to thrombotic complications, such as plaque rupture and blood clot formation. Experimental studies have shown that inflammation can drive arterial hyperplasia, even in the absence of traditional risk factors. The role of cytokines, adhesion molecules, and chemokines in recruiting inflammatory cells to the arterial wall has been elucidated, providing insights into the initiation and progression of atherosclerosis. Inflammation is also involved in the death of cells within atherosclerotic plaques, such as macrophages and smooth muscle cells, which can lead to the formation of a necrotic core. This core is a key factor in plaque instability and the risk of thrombosis. The heterogeneity of mononuclear phagocytes in atherosclerosis has been shown to influence disease progression, with certain subsets of macrophages playing a pro-inflammatory role. Adaptive and innate immune responses, including T cells and B cells, also contribute to atherosclerosis, with T cells playing a critical role in regulating inflammation. Allograft arteriopathy, a special form of atherosclerosis in transplant recipients, highlights the role of immune responses in the disease process. The translation of these findings to clinical practice has led to the use of biomarkers such as C-reactive protein (CRP) to assess cardiovascular risk. Statin drugs, which lower LDL cholesterol, also reduce inflammation, as evidenced by lower CRP levels. Clinical trials, such as the JUPITER study, have demonstrated the benefits of statin therapy in reducing cardiovascular events, even in individuals with low LDL levels. Ongoing research aims to further understand the role of inflammation in atherosclerosis and to develop new therapies targeting immune pathways. The integration of inflammation into the understanding of atherosclerosis has provided new insights into the disease and has led to improved risk assessment and treatment strategies.Inflammation plays a central role in the development of atherosclerosis, a condition characterized by the buildup of cholesterol and other substances in the arteries. Initially viewed as a cholesterol storage disease, atherosclerosis has been redefined through research showing that inflammation is a key driver of the disease. The discovery of immune mechanisms in atherosclerosis, such as the role of macrophages and inflammatory cells, has transformed understanding of the disease. Inflammation not only promotes plaque formation but also contributes to thrombotic complications, such as plaque rupture and blood clot formation. Experimental studies have shown that inflammation can drive arterial hyperplasia, even in the absence of traditional risk factors. The role of cytokines, adhesion molecules, and chemokines in recruiting inflammatory cells to the arterial wall has been elucidated, providing insights into the initiation and progression of atherosclerosis. Inflammation is also involved in the death of cells within atherosclerotic plaques, such as macrophages and smooth muscle cells, which can lead to the formation of a necrotic core. This core is a key factor in plaque instability and the risk of thrombosis. The heterogeneity of mononuclear phagocytes in atherosclerosis has been shown to influence disease progression, with certain subsets of macrophages playing a pro-inflammatory role. Adaptive and innate immune responses, including T cells and B cells, also contribute to atherosclerosis, with T cells playing a critical role in regulating inflammation. Allograft arteriopathy, a special form of atherosclerosis in transplant recipients, highlights the role of immune responses in the disease process. The translation of these findings to clinical practice has led to the use of biomarkers such as C-reactive protein (CRP) to assess cardiovascular risk. Statin drugs, which lower LDL cholesterol, also reduce inflammation, as evidenced by lower CRP levels. Clinical trials, such as the JUPITER study, have demonstrated the benefits of statin therapy in reducing cardiovascular events, even in individuals with low LDL levels. Ongoing research aims to further understand the role of inflammation in atherosclerosis and to develop new therapies targeting immune pathways. The integration of inflammation into the understanding of atherosclerosis has provided new insights into the disease and has led to improved risk assessment and treatment strategies.