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Novel insights of secretory phospholipase a(2) action in cardiology.

机译:心脏病中分泌性磷脂酶a(2)作用的新颖见解。

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Phospholipase A(2)s (PLA(2)s) produce free fatty acid and lysophospholipid from membrane phospholipid, and these products can be converted into various types of proinflammatory lipid mediators by specific enzymes. Among several types of PLA(2), secretory PLA(2)s (sPLA(2)s) have crucial roles in the development of cardiovascular diseases. Circulating sPLA(2) is increasing in patients with coronary artery disease (CAD), and it can be a risk factor for CAD and a prognostic factor in those patients. Secretory PLA(2)s amplify the inflammatory responses in myocardial ischemia/reperfusion injury and fetal acute respiratory distress. In some animal experiments, sPLA(2)s can hydrolyze low-density lipoprotein and high-density lipoprotein and lead to progress of atherosclerotic plaques. Some inhibitor studies for sPLA(2) revealed that inhibition of sPLA(2) reduced the myocardial impairment after ischemia/reperfusion injury and progression of atherosclerotic plaque areas in animal models. Secretory PLA(2)s might be a new target for cardiovascular medicine.
机译:磷脂酶A(2)s(PLA(2)s)从膜磷脂产生游离脂肪酸和溶血磷脂,这些产物可以通过特定的酶转化为各种类型的促炎性脂质介体。在几种类型的PLA(2)中,分泌型PLA(2)s(sPLA(2)s)在心血管疾病的发展中具有至关重要的作用。冠状动脉疾病(CAD)患者的循环sPLA(2)升高,并且可能是CAD的危险因素和这些患者的预后因素。分泌型PLA(2)会放大心肌缺血/再灌注损伤和胎儿急性呼吸窘迫中的炎症反应。在一些动物实验中,sPLA(2)s可以水解低密度脂蛋白和高密度脂蛋白,并导致动脉粥样硬化斑块的进展。一些针对sPLA(2)的抑制剂研究表明,抑制sPLA(2)可以减少动物模型中缺血/再灌注损伤和动脉粥样硬化斑块区域发展后的心肌损伤。分泌型PLA(2)可能是心血管医学的新目标。

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