ArticleCommunications biology2025
Mice develop obesity and lose myocardial metabolic flexibility months after exertional heat stroke.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Exertional heat stroke-related acute kidney injury: novel animal and cellular models.Renal failure · 2026Article
- Stroke Heart Syndrome: Neuroimmune and Metabolic Crosstalk with Conceptual Approaches for Precision Therapeutics.Cardiovascular drugs and therapy · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
As global temperatures rise, heat-related chronic health disorders are predicted to become more prevalent. We tested whether a single exposure to acute heat illness, using a preclinical mouse model of exertional heat stroke (EHS), can induce late-emerging health disorders that progress into chronic disease. Following EHS, mice were followed for 3 months; after two weeks of recovery, half were placed on a Western diet to determine if previous EHS exposure amplifies the negative consequences of an atherogenic diet. When compared to sham exercise controls, EHS-exposed mice exhibit accelerated diet-induced obesity, develop low level cardiac hypertrophy, develop accelerated diet-induced liver steatosis, severe hypoproteinemia and a loss of metabolic flexibility in the myocardium. The latter is characterized by a shift towards predominant glucose metabolism and glycolysis. These results demonstrate that a single exposure to severe exertional heat illness can induce long-lasting and unexpected health consequences in mammals and increased vulnerability to secondary metabolic stressors.
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