Key result
Continuous activation of gp130 in double-transgenic mice overexpressing IL-6 and IL-6R caused ventricular myocardial hypertrophy, increasing the heart-to-body weight ratio to 0.66% compared to 0.51% in controls (p<0.05).
Why the study?
Does continuous activation of gp130 cause myocardial hypertrophy in mice?
Population
Transgenic mice and in vitro neonatal heart muscle cells from normal mice
Comparison
Continuous activation of gp130 vs Transgenic mice overexpressing either IL-6 or…
Design
Preclinical
Follow-up
adulthood (for mice)
Authors
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Supports gp130-driven hypertrophy in mice; leaves open relevance to human cardiac disease.
Does continuous activation of gp130 cause myocardial hypertrophy in mice?
Absolute Event Rate: 0.66% vs 0.51%
p-value: p=<0.05
Continuous activation of the gp130 signaling pathway leads to cardiac hypertrophy, suggesting its involvement in the physiological regulation of the myocardium.
Hirota et al. (1995) studied Myocardial hypertrophy. Overexpression of IL-6 and IL-6R (Double-transgenic) vs. Single transgenic or non-transgenic mice was evaluated on Ratio of heart weight to body weight (%) (p=<0.05). Continuous activation of gp130 in double-transgenic mice overexpressing IL-6 and IL-6R caused ventricular myocardial hypertrophy, increasing the heart-to-body weight ratio to 0.66% compared to 0.51% in controls (p<0.05).
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