Abstract：
With global warming, extreme environmental heat is becoming a social issue of concern, which can cause adverse health results including heatstroke (HS). Severe heat stress is characterized by cell death of direct heat damage, excessive inflammatory responses, and coagulation disorders that can lead to multiple organ dysfunction (MODS) and even death. However, the significant pathophysiological mechanism and treatment of HS are still not fully clear. Various modes of cell death, including apoptosis, pyroptosis, ferroptosis, necroptosis and PANoptosis are involved in MODS induced by heatstroke. In this review, we summarized molecular mechanism, key transcriptional regulation as for HSF1, NRF2, NF-κB and PARP-1, and potential therapies of cell death resulting in CNS, liver, intestine, reproductive system and kidney injury induced by heat stress. Understanding the mechanism of cell death provides new targets to protect multi-organ function in HS.
摘要：
随着全球变暖,极端环境热正在成为社会关注的问题，这可能会导致不良的健康结果，包括中暑（HS）。严重的热应激的特征是直接热损伤的细胞死亡，过度的炎症反应，和可导致多器官功能障碍（MODS）甚至死亡的凝血障碍。然而,HS的重要病理生理机制和治疗仍不完全清楚。各种模式的细胞死亡，包括细胞凋亡,焦亡,铁性凋亡,中暑引起的MODS与坏死和PANoplast有关。在这次审查中,我们总结了分子机制，HSF1，NRF2，NF-κB和PARP-1的关键转录调控，以及导致CNS的细胞死亡的潜在疗法，肝脏,肠,热应激引起的生殖系统和肾脏损伤。了解细胞死亡的机制为保护HS的多器官功能提供了新的靶点。
