Heatstroke is a life-threatening condition caused by heat stress, which leads to circulatory failure and multiple organ dysfunctions. Heatstroke has become a more prevalent cause of death worldwide due to global warming. There are two types of heatstroke: classical heatstroke (CHS) and exertional heatstroke (EHS). CHS is caused by passive exposure to high temperatures and high humidity during heat waves, particularly among older individuals with preexisting illnesses. However, the majority of EHS cases occur in young, healthy individuals during vigorous exercise in hot or temperate environments. They are frequently observed in recreational and elite athletes, as well as military personnel. Heat acclimatization is the most effective way to prevent the occurrence of heatstroke.
With the development of critical care medicine, the clinical treatment of heatstroke patients has improved, but the mortality rate remains between 20 and 70%, and the heatstroke disability rate remains very high. According to previous studies, heatstroke and secondary multiple organ dysfunction syndromes (MODS) are caused by a complex interplay between the acute physiological changes associated with direct heat injuries, as well as the host’s inflammatory and coagulate responses. However, the underlying molecular mechanisms that cause heatstroke’s high mortality and disability rate are unknown, thus inhibiting the development of targeted and effective treatments. Further research into pathogenesis, particularly cellular and molecular pathologic mechanisms of heatstroke and heat acclimatization, is critical.
The current Research Topic will cover, but will not be limited to, the following subtopics:
1. The novel cellular and molecular mechanisms underlying heatstroke from onset to death, such as inflammation responses, immune dysfunction, endothelial injury, coagulation dysfunction, and so on;
2. The potential mechanisms of multiple organ injury during heatstroke, especially cell death, cell-cell interaction and molecular regulation;
3. Identify novel biomarkers for assessing the severity and prognosis of heatstroke;
4. Develop more accurate animal models or clinically novel predictive models or heat acclimatization models;
5. Basic and clinical research on developing new therapeutic strategies in addition to cooling treatment;
6. Heat acclimatization: Cellular, Molecular mechanisms, Enhancing techniques and methods.
Submissions are welcome for Original Research articles, Reviews, Mini-Reviews, and Perspectives.
Heatstroke is a life-threatening condition caused by heat stress, which leads to circulatory failure and multiple organ dysfunctions. Heatstroke has become a more prevalent cause of death worldwide due to global warming. There are two types of heatstroke: classical heatstroke (CHS) and exertional heatstroke (EHS). CHS is caused by passive exposure to high temperatures and high humidity during heat waves, particularly among older individuals with preexisting illnesses. However, the majority of EHS cases occur in young, healthy individuals during vigorous exercise in hot or temperate environments. They are frequently observed in recreational and elite athletes, as well as military personnel. Heat acclimatization is the most effective way to prevent the occurrence of heatstroke.
With the development of critical care medicine, the clinical treatment of heatstroke patients has improved, but the mortality rate remains between 20 and 70%, and the heatstroke disability rate remains very high. According to previous studies, heatstroke and secondary multiple organ dysfunction syndromes (MODS) are caused by a complex interplay between the acute physiological changes associated with direct heat injuries, as well as the host’s inflammatory and coagulate responses. However, the underlying molecular mechanisms that cause heatstroke’s high mortality and disability rate are unknown, thus inhibiting the development of targeted and effective treatments. Further research into pathogenesis, particularly cellular and molecular pathologic mechanisms of heatstroke and heat acclimatization, is critical.
The current Research Topic will cover, but will not be limited to, the following subtopics:
1. The novel cellular and molecular mechanisms underlying heatstroke from onset to death, such as inflammation responses, immune dysfunction, endothelial injury, coagulation dysfunction, and so on;
2. The potential mechanisms of multiple organ injury during heatstroke, especially cell death, cell-cell interaction and molecular regulation;
3. Identify novel biomarkers for assessing the severity and prognosis of heatstroke;
4. Develop more accurate animal models or clinically novel predictive models or heat acclimatization models;
5. Basic and clinical research on developing new therapeutic strategies in addition to cooling treatment;
6. Heat acclimatization: Cellular, Molecular mechanisms, Enhancing techniques and methods.
Submissions are welcome for Original Research articles, Reviews, Mini-Reviews, and Perspectives.
