What question did this study set out to answer?

Evaluate the therapeutic effects of TNF-alpha neutralization on myocardial inflammation and hypertrophy in a transgenic mouse model of cardiomyopathy.

May 30, 2000CirculationOpen Access

Soluble Tumor Necrosis Factor Receptor Abrogates Myocardial Inflammation but Not Hypertrophy in Cytokine-Induced Cardiomyopathy

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Why the study?

Does adenovirus-mediated neutralization of TNF-alpha improve myocardial inflammation and hypertrophy in a transgenic mouse model of cytokine-induced cardiomyopathy?

Population

6-week-old transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha

Comparison

Intravenous injection of an adenovirus encoding… vs Control mice

Design

Preclinical

Authors

TKToru KubotaSeirei Sakura Citizen Hospital GBGeorge S. BounoutasNovartis (Switzerland)MMMasayuki MiyagishimaTokyo Women's Medical University

Discussion

Member takes

Implication

May improve select LV parameters in inflammatory cardiomyopathy models without reversing hypertrophy; leaves open TNF-α neutralization as therapy in human HF.

Key Points

Evaluate the therapeutic effects of TNF-alpha neutralization on myocardial inflammation and hypertrophy in a transgenic mouse model of cardiomyopathy.
Injected adenovirus encoding TNF receptor-IgG fusion protein (AdTNFRI) intravenously into 6-week-old mice.
Measured TNFRI levels in plasma and myocardium after treatment.
Conducted echocardiographic measurements of left ventricular dimensions.
AdTNFRI abrogated myocardial inflammation, reducing expression of intercellular adhesion molecule-1 and downstream cytokines.
Left ventricular end-systolic diameter significantly decreased post-treatment compared to transgenic control mice.
Treatment did not reverse cardiomegaly or left ventricular wall thickening.

Structured PICO

Does adenovirus-mediated neutralization of TNF-alpha improve myocardial inflammation and hypertrophy in a transgenic mouse model of cytokine-induced cardiomyopathy?

Population

6-week-old transgenic mice with cardiac-specific overexpression of tumor necrosis factor (TNF)-alpha (model of dilated cardiomyopathy)

Intervention

Intravenous injection of an adenovirus encoding the 55-kDa TNF receptor-IgG fusion protein (AdTNFRI)

Comparator

Control mice

Outcome

Myocardial inflammation, cardiomegaly, and echocardiographic parameters (left ventricular end-systolic diameter and wall thickening)surrogate

Neutralization of TNF-alpha via AdTNFRI abrogates myocardial inflammation and improves LV end-systolic diameter but does not reverse hypertrophy in a mouse model of cytokine-induced cardiomyopathy.

Cite This Study

Kubota et al. (2000) studied this question.

synapsesocial.com/papers/6a135f8071369867e4937d7e https://doi.org/10.1161/01.cir.101.21.2518

Topics

Myocarditis

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Implication

May improve select LV parameters in inflammatory cardiomyopathy models without reversing hypertrophy; leaves open TNF-α neutralization as therapy in human HF.