Why the study?
Do S100A8 and S100A9 aggravate Coxsackievirus B3-induced myocarditis?
Population
Endomyocardial biopsies from patients with CVB3-positive myocarditis and controls; CVB3-infected wild-type…
Comparison
S100A9 knockout, exogenous S100A8 application… vs Wild-type mice, controls, and scrambled siRNA
Design
Preclinical
Key result
S100A8 and S100A9 aggravate Coxsackievirus B3-induced myocarditis, with S100A9 knockout mice showing improved left ventricular function and reduced viral load compared to wild-type mice.
Authors
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May identify S100A9 as a myocarditis target; hypothesis-generating, requiring human validation before any clinical consideration.
Do S100A8 and S100A9 aggravate Coxsackievirus B3-induced myocarditis?
p-value: p=0.038
S100A8 and S100A9 aggravate CVB3-induced myocarditis, suggesting they may serve as therapeutic targets in inflammatory cardiomyopathies.
Müller et al. (2017) studied Coxsackievirus B3-induced myocarditis. S100A8 and S100A9 vs. Controls / wild-type was evaluated on Left ventricular function and viral copy number (p=0.038). S100A8 and S100A9 aggravate Coxsackievirus B3-induced myocarditis, with S100A9 knockout mice showing improved left ventricular function and reduced viral load compared to wild-type mice.