Key result
ISG15 boosts ATP production and prevents cardiac atrophy during Coxsackievirus B3 infection by regulating glycolysis.
Why the study?
The molecular mechanisms by which the ISG15 system affects the functional properties of its protein substrates in the heart during Coxsackievirus B3 infection were unknown.
Does the ISG15 system preserve cardiac metabolism and function during Coxsackievirus B3 infection in mice?
Population
CVB3-infected mice and cardiomyocytes
Comparison
ISG15-/- vs competent ISG15 system
Design
Preclinical laboratory and animal study
Authors
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No immediate clinical implications for viral myocarditis; leaves open ISG15's metabolic role in human cardiac infection.
Does the ISG15 system preserve cardiac metabolism and function during Coxsackievirus B3 infection in mice?
Protein ISGylation by the ISG15 system protects against cardiac atrophy and dysfunction during viral myocarditis by reprogramming cardiac metabolism to preserve mitochondrial ATP production.
Bredow et al. (2024) studied this question. ISG15 enhances ATP production capacity and prevents cardiac atrophy during Coxsackievirus B3 infection by regulating glycolytic enzyme activity.
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