Thrombosis and hemostasis are critical processes that maintain vascular integrity, yet imbalances can lead to life-threatening cardiovascular events. Traditionally, erythrocytes were considered passive bystanders in coagulation, but emerging evidence highlights their active role in thrombogenesis, particularly through redox biology. Erythrocytes generate reactive oxygen and nitrogen species (RONS) via Hb autoxidation, NADPH oxidase activation, and external uptake from other blood components. This oxidative environment induces structural and functional modifications, including increased rigidity, phosphatidylserine exposure, microvesicle release, and enhanced adhesion to endothelial cells and platelets, all contributing to a prothrombotic phenotype. Hemorheological alterations such as increased aggregation and decreased deformability further exacerbate blood stasis and thrombus formation. Oxidative stress also accelerates hemolysis, releasing free Hb and heme, which trigger inflammatory responses and endothelial dysfunction, further amplifying thrombogenic potential. Additionally, erythrocyte-derived microvesicles act as carriers of procoagulant factors, enhancing thrombin generation and fibrin network formation. These mechanisms underscore the erythrocyte-ROS axis as a crucial determinant of thrombosis. Despite these insights, the full scope of erythrocyte-mediated redox signaling in thrombotic processes remains incompletely understood. This review discusses the multifaceted impact of erythrocyte oxidative stress on thrombosis and hemostasis, exploring its implications in cardiovascular diseases, metabolic disorders, and hematological conditions. Understanding these pathways may lead to novel therapeutic approaches targeting erythrocyte redox homeostasis to mitigate thrombotic risk and improve patient outcomes.