Scholarlink

<p>Global warming is leading to a continuous increase in the incidence of heat-related illnesses, among which heat stroke is the most severe type, characterized by a core body temperature &gt; 40&#xa0;°C and multiple organ dysfunction syndrome (MODS). The liver, being a thermosensitive organ, acts both as a target of injury and an "amplifier" of inflammation. Its acute injury and failure are significant causes of death in heat stress. This review summarizes the core mechanisms of heat stress-induced liver injury, including direct damage to hepatocytes by hyperthermia, the dual regulatory role of heat shock proteins (HSPs), gut barrier damage leading to endotoxemia and systemic inflammatory response, ischemia–reperfusion injury, and the involvement of various cell death modes such as apoptosis, pyroptosis, and ferroptosis. Clinically, liver injury manifests as a sharp rise in transaminases, abnormal bilirubin metabolism, and coagulation dysfunction, often combined with damage to the heart, brain, kidneys, and other organs, constituting MODS. Current treatments primarily focus on rapid cooling and organ support. Potential strategies include cell death inhibitors, antioxidants, and gut barrier protection. Severe cases may require artificial liver support systems (ALSS) or liver transplantation. Future efforts should delve deeper into the mechanisms of cell death, promote the clinical translation of targeted therapies, and strengthen effective prevention of heat stroke.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Heat stroke and the liver: mechanisms of injury and therapeutic strategies

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月13日

查看全文
  • Jinying Dou,
  • Qi Cui,
  • Wei Li,
  • Keran Jia,
  • Fukun Wang

摘要

Global warming is leading to a continuous increase in the incidence of heat-related illnesses, among which heat stroke is the most severe type, characterized by a core body temperature > 40 °C and multiple organ dysfunction syndrome (MODS). The liver, being a thermosensitive organ, acts both as a target of injury and an "amplifier" of inflammation. Its acute injury and failure are significant causes of death in heat stress. This review summarizes the core mechanisms of heat stress-induced liver injury, including direct damage to hepatocytes by hyperthermia, the dual regulatory role of heat shock proteins (HSPs), gut barrier damage leading to endotoxemia and systemic inflammatory response, ischemia–reperfusion injury, and the involvement of various cell death modes such as apoptosis, pyroptosis, and ferroptosis. Clinically, liver injury manifests as a sharp rise in transaminases, abnormal bilirubin metabolism, and coagulation dysfunction, often combined with damage to the heart, brain, kidneys, and other organs, constituting MODS. Current treatments primarily focus on rapid cooling and organ support. Potential strategies include cell death inhibitors, antioxidants, and gut barrier protection. Severe cases may require artificial liver support systems (ALSS) or liver transplantation. Future efforts should delve deeper into the mechanisms of cell death, promote the clinical translation of targeted therapies, and strengthen effective prevention of heat stroke.