ArticleFrontiers in immunology2023
Endothelial glycocalyx injury is involved in heatstroke-associated coagulopathy and protected by N-acetylcysteine.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Histopathological and molecular mechanisms of multi-organ damage in heat stroke: Endothelial failure, immune crosstalk, and regulated cell death pathways.Histology and histopathology · 2026Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Porphyromonas gingivalis-derived outer membrane vesicles promote vascular endothelial glycocalyx injury via the PPAD/CitH3/B3GAT1 pathway.Journal of nanobiotechnology · 2026Article
- Nuclear factor erythroid 2-related factor 2 gene expression in patients with heat stroke and its association with oxidative stress and inflammation: a prospective study.Frontiers in immunology · 2026Article
- A New Paradigm for Precision Medicine in Heatstroke: From Molecular Subtyping to Targeted Prevention and Treatment.Journal of inflammation research · 2026Review
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
- Sepsis and heatstroke: overlapping and distinct mechanisms of systemic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Impact of hyper- and hypothermia on cellular and whole-body physiology.Journal of intensive care · 2025Review
- Heat stroke dysfunctions: from pathophysiology to prediction.Frontiers in physiology · 2025Review
- The pathogenesis and management of heatstroke and heatstroke-induced lung injury.Burns & trauma · 2025Review
- The pathogenesis and therapeutic strategies of heat stroke-induced endothelial injury.Frontiers in cell and developmental biology · 2025Review
- High Glucose Induces Oxidative Stress That Alters Glycocalyx Proteoglycan Levels in Primary Rat Retinal Microvascular Endothelial Cells and in Isolated Ophthalmic Arteries.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- Article
- How can heatstroke damage the brain? A mini review.Frontiers in neuroscience · 2024Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Damage to endothelial glycocalyx (EGCX) can lead to coagulation disorders in sepsis. Heat stroke (HS) resembles sepsis in many aspects; however, it is unclear whether EGCX injury is involved in its pathophysiology. The purpose of this study was to examine the relationship between the damage of EGCX and the development of coagulation disorders during HS. Methods: We retrospectively collected 159 HS patients and analyzed coagulation characteristics and prognosis of HS patients with or without disseminated intravascular coagulation (DIC). We also replicated a rat HS model and measured coagulation indexes, pulmonary capillary EGCX injury in HS rats. Finally, we evaluated the effect of the antioxidant N-acetylcysteine (NAC) on HS-initiated EGCX injury and coagulation disorders. Results: Clinical data showed that HS patients complicated with DIC had a higher risk of death than HS patients without DIC. In a rat HS model, we found that rats subjected to heat stress developed hypercoagulability and platelet activation at the core body temperature of 43°C, just before the onset of HS. At 24 h of HS, the rats showed a consumptive hypo-coagulation state. The pulmonary capillary EGCX started to shed at 0 h of HS and became more severe at 24 h of HS. Importantly, pretreatment with NAC substantially alleviated EGCX damage and reversed the hypo-coagulation state in HS rats. Mechanically, HS initiated reactive oxidative species (ROS) generation, while ROS could directly cause EGCX damage. Critically, NAC protected against EGCX injury by attenuating ROS production in heat-stressed or hydrogen peroxide (H Discussion: Our results indicate that the poor prognosis of HS patients correlates with severe coagulation disorders, coagulation abnormalities in HS rats are associated with the damage of EGCX, and NAC improves HS-induced coagulopathy, probably through its protection against EGCX injury by preventing ROS generation.
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