Key result
CD36 deficiency in mice resulted in a significantly lower survival rate (p=0.0018) and impaired cardiac systolic function under pressure overload compared to wild-type mice.
Why the study?
The molecular mechanisms and functional role of the long-chain fatty acid transporter CD36 in the myocardium remain unknown.
Does pressure overload induced by transverse aortic constriction impair cardiac function and survival in CD36-knockout mice compared to wild-type mice?
Does pressure overload induced by transverse aortic constriction impair cardiac function and survival in CD36-knockout mice compared to wild-type mice?
p-value: p=0.0018
CD36 deficiency impairs tolerance to pressure overload in mice, leading to eccentric hypertrophy, fibrosis, and decreased ATP levels, highlighting the importance of long-chain fatty acid transporters in maintaining myocardial energy and function under stress.
CD36 supports myocardial energy provision and systolic function under pressure overload; leaves open therapeutic targeting in human cardiomyopathy.
CD36 is one of the important transporters of long-chain fatty acids (LCFAs) in the myocardium. We previously reported that CD36-deficient patients demonstrate a marked reduction of myocardial uptake of LCFA, while myocardial glucose uptake shows a compensatory increase, and are often accompanied by cardiomyopathy. However, the molecular mechanisms and functional role of CD36 in the myocardium remain unknown.The current study aimed to explore the pathophysiological role of CD36 in the heart. Methods: Using wild type (WT) and knockout (KO) mice, we generated pressure overload by transverse aortic constriction (TAC) and analyzed cardiac functions by echocardiography. To assess cardiac hypertrophy and fibrosis, histological and molecular analyses and measurement of ATP concentration in mouse hearts were performed.By applying TAC, the survival rate was significantly lower in KO than that in WT mice. After TAC, KO mice showed significantly higher heart weight-to-tibial length ratio and larger cross-sectional area of cardiomyocytes than those of WT. Although left ventricular (LV) wall thickness in the KO mice was similar to that in the WT mice, the KO mice showed a significant enlargement of LV cavity and reduced LV fractional shortening compared to the WT mice with TAC. A tendency for decreased myocardial ATP concentration was observed in the KO mice compared to the WT mice after TAC operation.These data suggest that the LCFA transporter CD36 is required for the maintenance of energy provision, systolic function, and myocardial structure.
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Nakatani et al. (2018) studied Pressure overload-induced heart failure. CD36 deficiency vs. Wild type (WT) mice was evaluated on Survival rate after severe transverse aortic constriction (p=0.0018). CD36 deficiency in mice resulted in a significantly lower survival rate (p=0.0018) and impaired cardiac systolic function under pressure overload compared to wild-type mice.
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