【摘 要】
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Objective Epoxyeicosatrienoic acids (EETs) limit mitochondrial damage, enhance post-ischemic cardiac functional recovery, and limit progression of cardiac hypertrophy in experimental models.The altere
【机 构】
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Animal Models for Cardiovascular Research Group, Guangdong Laboratory Animal Monitoring Institute ,
【出 处】
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第17届中国南方国际心血管病学术会议
论文部分内容阅读
Objective Epoxyeicosatrienoic acids (EETs) limit mitochondrial damage, enhance post-ischemic cardiac functional recovery, and limit progression of cardiac hypertrophy in experimental models.The altered EET metabolism is associated with a high risk of CAD in humans.Cardioprotective effects of EETs toward acute myocardial ischemia-reperfusion injury have been recognized ; however, the precise mechanism (s)are still largely unknown.Our objective is to understand whether EETs can prevent the development of heart failure and preserve cardiac function in myocardial infarction.An inhibition of sEH by a pharmacological agent or a gene deletion approach was used to fulfill our aims in a surgical myocardial infarction model.
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