Key result
Both pre- and post-MI treatments with AdTNFR1 were deleterious in a mouse MI model, promoting ventricular rupture or exacerbating ventricular dysfunction and remodeling.
Why the study?
Does soluble TNF receptor treatment prevent adverse outcomes in a mouse model of myocardial infarction?
Population
Mouse model of myocardial infarction induced by left coronary artery ligation
Comparison
Intravenous injection of adenovirus encoding a… vs Intravenous injection of adenovirus encoding LacZ
Design
Preclinical
Authors
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May support TNF neutralization in preclinical MI models; leaves open translation to human therapy after prior trial failures.
Does soluble TNF receptor treatment prevent adverse outcomes in a mouse model of myocardial infarction?
Neutralization of TNF-alpha via soluble TNF receptors is deleterious in a mouse MI model, suggesting TNF-alpha plays a protective role post-MI, which may explain the failure of anti-TNF therapies in clinical trials.
Monden et al. (2006) studied Myocardial infarction. AdTNFR1 (adenovirus encoding a 55-kDa TNF receptor-IgG fusion protein) vs. AdLacZ (adenovirus encoding LacZ) was evaluated on Ventricular rupture, remodeling, and dysfunction. Both pre- and post-MI treatments with AdTNFR1 were deleterious in a mouse MI model, promoting ventricular rupture or exacerbating ventricular dysfunction and remodeling.
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