Disturbed flow patterns in the vascular system significantly influence vascular endothelial cell (EC) function and contribute to the development of vascular diseases such as atherosclerosis, thrombosis, and venous insufficiency. In straight arterial segments, blood flow is typically laminar with high shear stress, promoting protective EC gene expression. In contrast, disturbed flow in arterial branches, curvatures, and post-stenotic regions results in low, reciprocating shear stress, which upregulates atherogenic genes and promotes atherosclerosis. Disturbed flow also contributes to postsurgical neointimal hyperplasia and clinical conditions like in-stent restenosis, vein bypass graft failure, and aortic valve calcification. In the venous system, disturbed flow due to reflux, outflow obstruction, or stasis leads to venous inflammation and thrombosis, causing chronic venous diseases. Understanding the effects of disturbed flow on ECs provides insights into the molecular mechanisms underlying vascular pathologies and helps elucidate the differences between quiescent and activated ECs. This review summarizes the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. It discusses the mechanisms by which disturbed flow induces endothelial dysfunction, including changes in shear stress, EC signaling, and gene expression. The review also highlights the importance of disturbed flow in the development of atherosclerosis, thrombosis, and other vascular diseases, and its relevance to clinical interventions. The study of disturbed flow in vitro using flow chambers and other models has provided valuable insights into the effects of disturbed flow on ECs and their responses to different shear stress patterns. These findings have important implications for the prevention and treatment of vascular diseases.Disturbed flow patterns in the vascular system significantly influence vascular endothelial cell (EC) function and contribute to the development of vascular diseases such as atherosclerosis, thrombosis, and venous insufficiency. In straight arterial segments, blood flow is typically laminar with high shear stress, promoting protective EC gene expression. In contrast, disturbed flow in arterial branches, curvatures, and post-stenotic regions results in low, reciprocating shear stress, which upregulates atherogenic genes and promotes atherosclerosis. Disturbed flow also contributes to postsurgical neointimal hyperplasia and clinical conditions like in-stent restenosis, vein bypass graft failure, and aortic valve calcification. In the venous system, disturbed flow due to reflux, outflow obstruction, or stasis leads to venous inflammation and thrombosis, causing chronic venous diseases. Understanding the effects of disturbed flow on ECs provides insights into the molecular mechanisms underlying vascular pathologies and helps elucidate the differences between quiescent and activated ECs. This review summarizes the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. It discusses the mechanisms by which disturbed flow induces endothelial dysfunction, including changes in shear stress, EC signaling, and gene expression. The review also highlights the importance of disturbed flow in the development of atherosclerosis, thrombosis, and other vascular diseases, and its relevance to clinical interventions. The study of disturbed flow in vitro using flow chambers and other models has provided valuable insights into the effects of disturbed flow on ECs and their responses to different shear stress patterns. These findings have important implications for the prevention and treatment of vascular diseases.