Macrophages play a critical role in the development and progression of cardiovascular diseases (CVD) by influencing inflammation, tissue repair, and fibrosis. They are multifunctional innate immune cells that respond to cardiovascular injury by recruiting to the damaged area, where they secrete pro-inflammatory and anti-inflammatory mediators, stimulate extracellular matrix (ECM) production, and regulate fibrosis. Macrophages exhibit diverse phenotypes and functions depending on the disease context, with M1 and M2 subsets representing pro-inflammatory and anti-inflammatory roles, respectively. However, in vivo, macrophages are more heterogeneous, with tissue-resident and monocyte-derived macrophages showing distinct functions. In cardiac diseases, macrophages contribute to myocardial fibrosis, which is a common pathological outcome of various CVD. In vascular diseases, inflammation leads to vascular injury, thrombosis, and CVD such as myocardial infarction (MI). Recent advances in single-cell sequencing technologies have revealed macrophage heterogeneity, cell-cell interactions, and therapeutic targets at a higher resolution, providing new insights into macrophage-mediated mechanisms in CVD. This review summarizes the diverse phenotypic and functional plasticity of macrophages in CVD, focusing on different causes and characteristics of diseases, especially the relationship between inflammation and fibrosis in cardiac diseases (myocardial infarction, pressure overload, myocarditis, dilated cardiomyopathy, diabetic cardiomyopathy, and cardiac aging) and the relationship between inflammation and vascular injury in vascular diseases (atherosclerosis and aneurysm). It also highlights preclinical and clinical macrophage targeting strategies and their translational implications. Macrophages are essential contributors to the development of various CVD, and their regulation is crucial for effective CVD therapy. The review discusses the origin, phenotype, and function of macrophages in the cardiovascular system, emphasizing their roles in inflammation, fibrosis, and tissue repair. It also explores the heterogeneity and regulatory mechanisms of cardiac macrophages, focusing on ischemic injury, chronic myocardial infarction, and ischemia-reperfusion injury. The review highlights the complex interplay between macrophages and other cells in the context of CVD, providing new intervention targets and therapeutic strategies for the clinical treatment of CVD.Macrophages play a critical role in the development and progression of cardiovascular diseases (CVD) by influencing inflammation, tissue repair, and fibrosis. They are multifunctional innate immune cells that respond to cardiovascular injury by recruiting to the damaged area, where they secrete pro-inflammatory and anti-inflammatory mediators, stimulate extracellular matrix (ECM) production, and regulate fibrosis. Macrophages exhibit diverse phenotypes and functions depending on the disease context, with M1 and M2 subsets representing pro-inflammatory and anti-inflammatory roles, respectively. However, in vivo, macrophages are more heterogeneous, with tissue-resident and monocyte-derived macrophages showing distinct functions. In cardiac diseases, macrophages contribute to myocardial fibrosis, which is a common pathological outcome of various CVD. In vascular diseases, inflammation leads to vascular injury, thrombosis, and CVD such as myocardial infarction (MI). Recent advances in single-cell sequencing technologies have revealed macrophage heterogeneity, cell-cell interactions, and therapeutic targets at a higher resolution, providing new insights into macrophage-mediated mechanisms in CVD. This review summarizes the diverse phenotypic and functional plasticity of macrophages in CVD, focusing on different causes and characteristics of diseases, especially the relationship between inflammation and fibrosis in cardiac diseases (myocardial infarction, pressure overload, myocarditis, dilated cardiomyopathy, diabetic cardiomyopathy, and cardiac aging) and the relationship between inflammation and vascular injury in vascular diseases (atherosclerosis and aneurysm). It also highlights preclinical and clinical macrophage targeting strategies and their translational implications. Macrophages are essential contributors to the development of various CVD, and their regulation is crucial for effective CVD therapy. The review discusses the origin, phenotype, and function of macrophages in the cardiovascular system, emphasizing their roles in inflammation, fibrosis, and tissue repair. It also explores the heterogeneity and regulatory mechanisms of cardiac macrophages, focusing on ischemic injury, chronic myocardial infarction, and ischemia-reperfusion injury. The review highlights the complex interplay between macrophages and other cells in the context of CVD, providing new intervention targets and therapeutic strategies for the clinical treatment of CVD.