MINI REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1668203
This article is part of the Research TopicImmune Landscape in the Transition from Inflammation to TumorigenesisView all 5 articles
Endothelial Activation in Thromboangiitis Obliterans: Mechanisms and Therapeutic Horizons
Provisionally accepted
- 1National Chinmedomics Research Center, Metabolomics Laboratory, Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin 150040, China., Harbin, China
- 2Vascular Surgery Department, Harbin Fifth Hospital, China., Harbin, China
- 3Department of Peripheral Vascular Disease. First Affilliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150006, China., Harbin, China
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Thromboangiitis obliterans (TAO) is a non-atherosclerotic, inflammatory vasculopathy characterized by thrombotic occlusion of small-and medium-sized vessels, leading to tissue ischemia and gangrene. Emerging evidence underscores endothelial cell (EC) activation as a central driver of disease progression, mediated by immune dysregulation, oxidative stress (Nrf2/ROS imbalance), impaired nitric oxide signaling (eNOS/iNOS dysregulation), endoplasmic reticulum and mitochondrial dysfunction, and disrupted copper/iron homeostasis. These pathways collectively promote a prothrombotic, proinflammatory endothelial phenotype, perpetuating vascular injury. Current therapies primarily alleviate symptoms but fail to address underlying EC dysfunction. Recent advances, including stem cell therapy and targeted immunomodulation, offer promising avenues for restoring endothelial homeostasis. However, translating mechanistic insights into durable clinical benefits requires further research into precision medicine approaches and large-scale validation of novel therapeutics. This review summarizes the multifactorial pathogenesis of TAO, emphasizing EC activation as a therapeutic linchpin, and outlines future directions to bridge translational gaps in disease management.
Keywords: Thromboangiitis Obliterans, endothelial cell, Immune dysregulation, Mitochondrial dysfunction, Copper/iron homeostasis, Thrombogenicity, Therapeutic interventions
Received: 17 Jul 2025; Accepted: 13 Aug 2025.
Copyright: © 2025 Wang, Chang and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Gang Zhao, Department of Peripheral Vascular Disease. First Affilliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150006, China., Harbin, China
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