【摘 要】
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Background Epoxyeicosatrienoic acids (EETs), hydrolyzed and degraded by soluble epoxide hydrolase (sEH) have been shown to attenuate cardiac hypertrophy induced
【机 构】
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DepartmentofCardiology,SunYat-senMemorialHospitalofSunYat-senUniversity,Guangzhou,China
【出 处】
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2014 International Symposium on Polyunsaturated Fatty Acids
论文部分内容阅读
Background Epoxyeicosatrienoic acids (EETs), hydrolyzed and degraded by soluble epoxide hydrolase (sEH) have been shown to attenuate cardiac hypertrophy induced by pressure overload.However, the mechanism in not fully understood, especially in simple mechanical stretch-induced cardiac hypertrophy.Mitochondrial dysfunction and injury might be a key factor in the deterioration process of cardiac hypertrophy.It was demonstrated that adenine nucleotide translocase 1(ANT1), a multifunctional protein in heart that facilitates the transport of ADP and ATP across the inner mitochondrial membrane, appeared to prevent the process of myocardial remodeling and cardiac insufficiency.In this study, we try to determine whether deletion of sEH attenuates cardiac hypertrophy during mechanical stretch via maintaining mitochondrial function and whether sEH deletion benefits mitochondria via upregulation cardiac ANT1 expression.
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