• Ping Wang, Lin Zheng, Sheng Yan, Xuezhen Xuan, Yusi Yang, Xiaotong Qi, and Honglin Dong.
• Department of Vascular Surgery, The Second Hospital, Shanxi Medical University, Taiyuan 030001, China; Department of Radiology, Mayo Clinic, Rochester, MN, United States.
• Am. J. Med. Sci. 2024 May 1; 367 (5): 296303296-303.

AbstractTraditionally, red blood cells (RBCs) have been perceived as passive entities within the fibrin network, without any significant role in the pathophysiology of venous thromboembolism (VTE). This review explores the involvement of RBCs in the VTE process, summarizing previous study findings and providing a comprehensive review of the latest theories. At first, it explores the influence of abnormal RBC counts (as seen in polycythemia vera and with erythropoietin use) and the exposure of RBCs to phosphatidylserine (Ptd-L-Ser) in the pathophysiology of VTE. The mechanisms of endothelial injury induced by RBCs and their adhesion to the endothelium under different disease models are then demonstrated. We explore the role of physical and chemical interactions between RBCs and platelets, as well as the interactions between RBCs and neutrophils - particularly the neutrophil extracellular traps (NETs) released by neutrophils - in the process of VTE. Additionally, we investigate the effect of RBCs on thrombin activation through two pathways, namely, the FXIIa-FXI-FIX pathway and the prekallikrein-dependent pathway. Lastly, we discuss the impact of RBCs on clot volume. In conclusion, we propose several potential methods aimed at unraveling the role of RBCs and their interaction with other components in the vascular system in the pathogenesis of VTE.Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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