Research Advances in the Mechanism of Mitochondrial Damage in Heatstroke

Corresponding author: lijieping, liejieping@yeah.net

DOI: 10.12201/bmr.202410.00030

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  Abstract: Heat stroke (HS), also known as severe heat stroke, is a severe thermoregulatory imbalance in the body due to thermal injury factors such as exposure to a hot environment or strenuous exercise, characterized by hyperthermia, a rapid increase in core body temperature (more than 40°C), systemic inflammatory response, central nervous system dysfunction (e.g., delirium, convulsions, or coma, etc.), and multiorgan failure (e.g., liver, intestines, and lungs, etc.). Acute heat-related illnesses have a high morbidity and mortality rate 1-2.HS is the most severe type of heat-related illness, and its pathogenic mechanism is still unclear, and is mostly thought to be caused by a complex interaction between heat-related cytotoxicity, inflammation, and disseminated intravascular coagulation 3. Systemic Inflammatory Response Syndrome (SIRS), activated secondary to heat stress, is thought to be the primary pathologic mechanism for the development of HS. Mitochondria play an important role in controlling the inflammator

  Key words: Heat stroke; Mitochondria; Heat stress; Mechanisms of damage

  Submit time: 11 October 2024

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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