REVIEW article
Front. Cell Dev. Biol.
Sec. Signaling
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1569346
This article is part of the Research TopicTargeting Pulmonary Endothelium in Acute Lung Injury and Acute Respiratory Distress SyndromeView all 11 articles
The pathogenesis and therapeutic strategies of heat stroke-induced endothelial injury
Provisionally accepted
- Changhai Hospital, Second Military Medical University, Shanghai, China
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Heat stroke is a severe and life-threatening condition characterized by elevated core body temperature and central nervous system dysfunction, often accompanied by multi-organ damage. The incidence and mortality of heat stroke are increasing due to global warming and more frequent heatwaves. This review aims to summarize the recent progress in understanding the pathogenesis of heat stroke-induced endothelial injury and explore potential therapeutic strategies. The vascular endothelium plays a crucial role in maintaining vascular homeostasis, and its dysfunction is a key factor in the development of heat stroke complications. The pathogenesis of heat stroke-induced endothelial injury involves multiple mechanisms, including degradation of the endothelial glycocalyx, impaired vascular tone regulation, disruption of intercellular junctional proteins, and activation of regulated cell death pathways. Biomarkers such as syndecan-1, endothelin-1, and von Willebrand factor are associated with endothelial injury and can predict disease severity and outcomes. Potential interventions include early fluid resuscitation, heat acclimation, and targeted therapies to inhibit specific cell death pathways or protect the endothelial glycocalyx. Further research is needed to elucidate the detailed mechanisms and develop targeted therapeutic interventions to reduce the morbidity and mortality of heat stroke.
Keywords: heat stroke, heat stress, endothelial dysfunction, vascular barrier, glycocalyx Abbreviations：HS, heat stroke, EC, Endothelial cell, ICAM-1, intercellular adhesion molecular-1, SDC-1, syndecan-1, ALI, Acute Lung Injury, ARDS, acute respiratory distress syndrome, DIC, disseminated intravascular coagulation, VCAM-1, vascular cell adhesion molecule-1
Received: 31 Jan 2025; Accepted: 16 Jun 2025.
Copyright: © 2025 Wang, Zhang, Zhang, Wang, Bo and Wang. 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:
Lulong Bo, Changhai Hospital, Second Military Medical University, Shanghai, China
Meitang Wang, Changhai Hospital, Second Military Medical University, Shanghai, China
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