Key result
Overexpression of IL-18 in fructose-fed rats significantly increased collagen volume fraction (8.43% vs 6.78%) and aggravated left ventricular diastolic dysfunction compared to control.
Why the study?
Does intravenous administration of an adenovirus encoding rat IL-18 aggravate left ventricular remodeling and diastolic dysfunction in male Wistar rats fed 10% fructose?
Population
Male Wistar rats receiving 10% fructose in water for 8 months (animal model for metabolic syndrome)
Design
Preclinical
Authors
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Hypothesis-generating for IL-18 inhibition in metabolic cardiomyopathy; human trials needed before clinical adoption.
Does intravenous administration of an adenovirus encoding rat IL-18 aggravate left ventricular remodeling and diastolic dysfunction in male Wistar rats fed 10% fructose?
Absolute Event Rate: 8.43% vs 6.78%
p-value: p=<0.05
Overexpression of IL-18 aggravates left ventricular remodeling and diastolic dysfunction in a rat model of metabolic syndrome, highlighting inflammation as a potential therapeutic target for metabolic cardiomyopathy.
Xing et al. (2010) studied Metabolic syndrome and cardiac fibrosis (n=43). Adenovirus carrying the IL-18 gene (Ad-IL-18) vs. Adenovirus containing the GFP gene (Ad-GFP) was evaluated on Collagen volume fraction (p=<0.05). Overexpression of IL-18 in fructose-fed rats significantly increased collagen volume fraction (8.43% vs 6.78%) and aggravated left ventricular diastolic dysfunction compared to control.
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