Cardiomyocyte‐Specific Ablation of the Long‐Chain Fatty Acid Transporter CD36 Accelerates the Progression of Pressure Overload‐Induced Heart Failure in Mice

Abstract only Utilizing an inducible cardiomyocyte‐specific CD36 knockout (icCD36KO) mouse, we investigated the pathophysiological role of myocardial fatty acid transporter CD36 in response to pressure overload and tested whether the ablation of CD36, used as a tool to limit fatty acid uptake and pa...

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Bibliographic Details
Published in:The FASEB journal 2015-04, Vol.29 (S1)
Main Authors: Sung, Miranda, Byrne, Nikole, Levasseur, Jody, Masson, Grant, Febbraio, Maria, Dyck, Jason
Format: Article
Language:English
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Summary:Abstract only Utilizing an inducible cardiomyocyte‐specific CD36 knockout (icCD36KO) mouse, we investigated the pathophysiological role of myocardial fatty acid transporter CD36 in response to pressure overload and tested whether the ablation of CD36, used as a tool to limit fatty acid uptake and partially inhibit fatty acid oxidation, would be beneficial or detrimental to cardiac function. Wildtype (WT) and icCD36KO mice were subjected to transverse aortic constriction (TAC) surgery to generate pressure overload‐induced cardiac hypertrophy. Following TAC, both WT and icCD36KO mice developed similar degrees of compensatory cardiac hypertrophy in response to pressure overload at 1, 3 and 5 weeks post‐TAC (N=7‐11/group). However, we observed significant systolic dysfunction and reduced ejection fraction (EF) in icCD36KO mice at 5 weeks post‐TAC (%EF: 52.4 ± 2.82 vs. 35.6 ± 3.01; P
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.29.1_supplement.lb593