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Updated: Mar 14, 2026
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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
Published on: July 14, 2016
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Age-related trade-offs: When protection becomes pathology
1Institute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, Scotland; School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand.
Cell Host & Microbe
|March 12, 2026
Summary
Cardiac Foxo1-Trim63 protects young mice from sepsis but increases mortality in aged mice. This study reveals how early disease tolerance mechanisms can harm late-life survival.
Area of Science:
- Immunology
- Cardiovascular Biology
- Aging Research
Background:
- The immune system balances pathogen resistance and disease tolerance during infection to minimize host damage.
- Understanding age-dependent immune responses is crucial for treating infections in diverse populations.
Purpose of the Study:
- To investigate the role of cardiac Foxo1-Trim63 in polymicrobial sepsis.
- To determine how age influences the protective or detrimental effects of this cardiac factor during sepsis.
Main Methods:
- Utilized young and aged mouse models to study polymicrobial sepsis.
- Examined the expression and function of Foxo1-Trim63 in cardiac tissue.
- Assessed survival rates and physiological parameters in response to infection.
Main Results:
- Cardiac Foxo1-Trim63 expression protected young mice against polymicrobial sepsis.
- In aged mice, cardiac Foxo1-Trim63 exacerbated sepsis, leading to increased mortality.
- Demonstrated a paradoxical role of this factor dependent on host age.
Conclusions:
- Cardiac Foxo1-Trim63 acts as a critical regulator of sepsis outcomes, with age-dependent effects.
- Early-life disease tolerance mechanisms involving cardiac Foxo1-Trim63 may compromise survival in aged individuals.
- Highlights the need for age-specific therapeutic strategies in infectious diseases.
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