Key result
Blockade of MyD88 using Ad5-dnMyD88 significantly reduced the heart weight to body weight ratio by 18.2% (0.36 vs 0.44) and cardiac myocyte apoptosis by 76.2% in rats with aortic banding.
Why the study?
Does blockade of MyD88 attenuate cardiac hypertrophy and decrease cardiac myocyte apoptosis in a rat model of pressure overload?
Population
Rat model of pressure overload-induced cardiac hypertrophy via aortic banding (n=32 total; 4 groups of 8)
Comparison
Adenovirus expressing dominant negative MyD88… vs Ad5-green fluorescent protein transfection +…
Design
Preclinical
Follow-up
3 weeks
Authors
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Does not support clinical use; extends preclinical evidence implicating MyD88 in pressure-overload remodeling.
Does blockade of MyD88 attenuate cardiac hypertrophy and decrease cardiac myocyte apoptosis in a rat model of pressure overload?
Effect estimate: 18.2% reduction
Absolute Event Rate: 0.36% vs 0.44%
In a rat model of pressure overload, blocking MyD88 significantly reduced cardiac hypertrophy and apoptosis while improving cardiac function, highlighting its role in the TLR4/NF-κB pathway.
Ha et al. (2005) studied Pressure overload-induced cardiac hypertrophy (n=32). Adenovirus expressing dominant negative MyD88 (Ad5-dnMyD88) vs. Ad5-GFP, aortic banding alone, and sham operation was evaluated on Heart weight to body weight (HW/BW) ratio (18.2% reduction). Blockade of MyD88 using Ad5-dnMyD88 significantly reduced the heart weight to body weight ratio by 18.2% (0.36 vs 0.44) and cardiac myocyte apoptosis by 76.2% in rats with aortic banding.
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