HomoarginineSupplementationPreventsLeftVentricularDilatationandPreservesSystolicFunctioninaModelofCoronaryArteryDiseaseJAHAresearch-articleJuly16,:8(14),e./JAHA..本文由“天纳”临床学术信息人工智能系统自动翻译点击文末“阅读原文”下载本文PDFBackgroundHomoarginine(hArg)hasbeenshowntobecardioprotectiveinamodelofischemicheartfailure;however,themechanismremainsunknown.hArgcaninhibittissue‐nonspecificalkalinephosphatase(TNAP),anenzymethatpromotesvascularcalcification.WehypothesizedthathArgwillexertbeneficialeffectsbyreducingcalcificationinamousemodelofcoronaryarterydiseaseassociatedwithTNAPoverexpressionandhypercholesterolemia.在缺血性心力衰竭模型中，高精氨酸（harg）已被证明具有心脏保护作用；然而，其机制仍不清楚。harg可抑制组织非特异性碱性磷酸酶（tnap），一种促进血管钙化的酶。我们假设，在一个与TNAP过度表达和高胆固醇血症相关的冠状动脉疾病的小鼠模型中，Harg将通过减少钙化发挥有益的作用。MethodsandResultsTNAPwasoverexpressedintheendotheliuminmicehomozygousforalow‐densitylipoproteinreceptormutation(wickedhighcholesterol[WHC]allele).WHCandWHC–endothelialTNAPmicereceivedplaceboorhArgsupplementation(14?mg/Lindrinkingwater)startingat6?weeksofagesimultaneouslywithanatherogenicdiet.Out
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