Key result
In mice subjected to 6 weeks of pressure overload, adiponectin deficiency prevented left ventricular chamber dilation and preserved systolic function and mitochondrial oxidative capacity compared to wild-type mice.
Why the study?
Does adiponectin deletion prevent adverse left ventricular remodeling and metabolic deterioration in mice subjected to prolonged pressure overload?
Population
Wild-type and adiponectin mice subjected to pressure overload via transverse aortic constriction
Comparison
Adiponectin deletion (adiponectin mice)… vs Wild-type mice subjected to prolonged transverse…
Design
Preclinical
Follow-up
6 weeks
Authors
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Adiponectin deletion may attenuate remodeling in pressure-overload mice; hypothesis-generating for human HF and should not change practice.
Does adiponectin deletion prevent adverse left ventricular remodeling and metabolic deterioration in mice subjected to prolonged pressure overload?
p-value: p=<0.05
Adiponectin deletion in mice subjected to prolonged pressure overload prevents LV chamber dilation and preserves mitochondrial oxidative capacity, suggesting adiponectin plays a permissive role in adverse cardiac remodeling.
O’Shea et al. (2010) studied Pressure overload-induced cardiac hypertrophy. Adiponectin deficiency vs. Wild-type mice was evaluated on Left ventricular remodeling and systolic function (end diastolic volume, end systolic volume, and ejection fraction) (p=<0.05). In mice subjected to 6 weeks of pressure overload, adiponectin deficiency prevented left ventricular chamber dilation and preserved systolic function and mitochondrial oxidative capacity compared to wild-type mice.
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