Impact of hyper- and hypothermia on cellular and whole-body physiology
Abstract 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 platel...
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| Language: | English |
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BMC
2025-01-01
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| Series: | Journal of Intensive Care |
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| Online Access: | https://doi.org/10.1186/s40560-024-00774-8 |
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| author | Toshiaki Iba Yutaka Kondo Cheryl L. Maier Julie Helms Ricard Ferrer Jerrold H. Levy |
| author_facet | Toshiaki Iba Yutaka Kondo Cheryl L. Maier Julie Helms Ricard Ferrer Jerrold H. Levy |
| author_sort | Toshiaki Iba |
| collection | DOAJ |
| description | Abstract 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. |
| format | Article |
| id | doaj-art-2b1e4cdd4ffd4d93b0e930475be9c1cf |
| institution | Kabale University |
| issn | 2052-0492 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Intensive Care |
| spelling | doaj-art-2b1e4cdd4ffd4d93b0e930475be9c1cf2025-01-19T12:11:58ZengBMCJournal of Intensive Care2052-04922025-01-0113111110.1186/s40560-024-00774-8Impact of hyper- and hypothermia on cellular and whole-body physiologyToshiaki Iba0Yutaka Kondo1Cheryl L. Maier2Julie Helms3Ricard Ferrer4Jerrold H. Levy5Department of Emergency and Disaster Medicine, Juntendo University Graduate School of MedicineDepartment of Emergency and Disaster Medicine, Juntendo University Graduate School of MedicineDepartment of Pathology and Laboratory Medicine, Emory University School of MedicineStrasbourg University (UNISTRA), Strasbourg University Hospital, Medical Intensive Care Unit-NHC; INSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine (RNM), FMTSIntensive Care Department, Hospital Universitari Vall d’Hebron Universitat Autònoma de BarcelonaDepartment of Anesthesiology, Critical Care, and Surgery, Duke University School of MedicineAbstract 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.https://doi.org/10.1186/s40560-024-00774-8HyperthermiaHypothermiaInflammationCoagulationCell death |
| spellingShingle | Toshiaki Iba Yutaka Kondo Cheryl L. Maier Julie Helms Ricard Ferrer Jerrold H. Levy Impact of hyper- and hypothermia on cellular and whole-body physiology Journal of Intensive Care Hyperthermia Hypothermia Inflammation Coagulation Cell death |
| title | Impact of hyper- and hypothermia on cellular and whole-body physiology |
| title_full | Impact of hyper- and hypothermia on cellular and whole-body physiology |
| title_fullStr | Impact of hyper- and hypothermia on cellular and whole-body physiology |
| title_full_unstemmed | Impact of hyper- and hypothermia on cellular and whole-body physiology |
| title_short | Impact of hyper- and hypothermia on cellular and whole-body physiology |
| title_sort | impact of hyper and hypothermia on cellular and whole body physiology |
| topic | Hyperthermia Hypothermia Inflammation Coagulation Cell death |
| url | https://doi.org/10.1186/s40560-024-00774-8 |
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