Key result
Cardiospecific CD36 inhibition protected against high-fat-diet induced cardiac remodeling by increasing left ventricular ejection fraction and decreasing heart-to-body weight ratio in obese mice.
Why the study?
Does cardiospecific CD36 suppression by lentivirus-mediated RNA interference prevent cardiac hypertrophy and systolic dysfunction in high-fat-diet induced obese mice?
Does cardiospecific CD36 suppression by lentivirus-mediated RNA interference prevent cardiac hypertrophy and systolic dysfunction in high-fat-diet induced obese mice?
Absolute Event Rate: 72.88% vs 70.25%
p-value: p=<0.05
Cardiospecific suppression of the fatty acid transporter CD36 prevents cardiac hypertrophy, systolic dysfunction, and myocardial lipid accumulation in a mouse model of obesity-related cardiomyopathy.
No takes yet. Share an insight, caveat, or question.
Cardiospecific CD36 suppression warrants no clinical consideration yet; leaves open therapeutic targeting in human obesity cardiomyopathy.
Zhang et al. (2015) studied Obesity-related cardiomyopathy (n=40). Cardiospecific CD36 suppression by lentivirus-mediated RNA interference vs. Irrelevant gene (GFP) silencing was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.05). Cardiospecific CD36 inhibition protected against high-fat-diet induced cardiac remodeling by increasing left ventricular ejection fraction and decreasing heart-to-body weight ratio in obese mice.
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