Key result
Transgenic overexpression of Angptl4 in the mouse heart inhibited cardiac lipoprotein lipase activity and increased fasting plasma triglyceride levels to 133.1 mg/dl compared to 58.4 mg/dl in controls.
Why the study?
Does transgenic overexpression of Angptl4 in the heart inhibit cardiac lipoprotein utilization and induce left-ventricular dysfunction in mice?
Population
Transgenic mice overexpressing Angptl4 in the heart and double transgenic mice overexpressing both Angptl4…
Comparison
Transgenic overexpression of Angptl4 in the heart vs Wild-type mice
Design
Preclinical
Authors
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Cardiac Angptl4 overexpression alters lipid handling in mice; leaves open relevance to human heart failure pathogenesis.
Does transgenic overexpression of Angptl4 in the heart inhibit cardiac lipoprotein utilization and induce left-ventricular dysfunction in mice?
Absolute Event Rate: 133.1% vs 58.4%
p-value: p=<0.0001
Overexpression of Angptl4 in the heart inhibits lipoprotein-derived fatty acid delivery and causes left-ventricular dysfunction, providing a model for studying heart failure pathogenesis.
Yu et al. (2005) studied Cardiomyopathy / Lipid metabolism. Transgenic overexpression of Angptl4 in the heart (MHC-Angptl4) vs. Wild-type littermates was evaluated on Fasting plasma triglyceride levels (mg/dl) (p=<0.0001). Transgenic overexpression of Angptl4 in the mouse heart inhibited cardiac lipoprotein lipase activity and increased fasting plasma triglyceride levels to 133.1 mg/dl compared to 58.4 mg/dl in controls.
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