Journal of intensive careReview
13 Jan 2025
The incidence of heat-related illnesses and heatstroke continues to rise amidst global warming. Hyperthermia triggers inflammation, coagulation, and progressive multiorgan dysfunction, and, at levels above 40 °C, can even lead to cell death.
Blood cells, particularly granulocytes and platelets, are highly sensitive to heat, which promotes proinflammatory and procoagulant changes. Key factors in heatstroke pathophysiology involve mitochondrial thermal damage and excessive oxidative stress, which drive apoptosis and necrosis.
While the kinetics of cellular damage from heat have been extensively studied, the mechanisms driving heat-induced organ damage and death are not yet fully understood. Converse to hyperthermia, hypothermia is generally protective, as seen in therapeutic hypothermia.
However, accidental hypothermia presents another environmental threat due to arrhythmias, cardiac arrest, and coagulopathy.
From a cellular physiology perspective, hypothermia generally supports mitochondrial homeostasis and enhances cell preservation, aiding whole-body recovery following resuscitation.
This review summarizes recent findings on temperature-related cellular damage and preservation and suggests future research directions for understanding the tempo-physiologic axis.
Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: T. Iba participated on advisory boards of Japan Blood Products Organization, Asahi Kasei Pharmaceuticals, and Toray Medical. J. Helms has received honoraria from Asahi Kasei Pharmaceuticals, Diagnostica Stago, Pfizer PFE France, Sanofi Aventis France, MSD, Shionogi, and Inotrem. J. H. Levy serves on the Steering or Advisory Grifols, Octapharma, Takeda, and Werfen. The other authors have no conflict of interest.
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