首页> 外文期刊>Cardiovascular pathology: the official journal of the Society for Cardiovascular Pathology >Syndecan-4 deficiency accelerates the transition from compensated hypertrophy to heart failure following pressure overload
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Syndecan-4 deficiency accelerates the transition from compensated hypertrophy to heart failure following pressure overload

机译:Syndecan-4缺乏在压力过载后加速了从补偿肥大到心力衰竭的过渡

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Increasing evidence suggests that a mismatch between angiogenesis and myocardial growth contributes to the transition from adaptive cardiac hypertrophy to heart failure following pressure overload. Syndecan-4 is a transmembrane proteoglycan that binds to growth factors and extracellular matrix proteins and is critical in focal adhesion formation. However, its effects on coronary angiogenesis during pressure overload-induced heart failure have not been studied. Here, we hypothesize that syndecan-4modulates cardiac remodeling in response to pressure overload through its ability to regulate adaptive angiogenesis. Syndecan-4 knockout (syndecan-4 KO) and wild-type (WT) mice were subjected to pressure overload induced by transverse aortic constriction (TAC). Syndecan-4 KO mice exhibited reduced capillary density, attenuated cardiomyocyte size, andworsened left ventricular cardiac function after TAC surgery compared with WT mice. Moreover, syndecan-4 KO mice showed a significant decrease in protein kinase C alpha expression. Our data suggest that syndecan-4 is essential for the compensated hypertrophy and the maintenance of cardiac function during the process of heart failure following pressure overload. (C) 2017 Published by Elsevier Inc.
机译:越来越多的证据表明血管生成和心肌生长之间的错配有助于在压力过载后从自适应心脏肥厚到心力衰竭的过渡。 Syndecan-4是跨膜蛋白多糖,其与生长因子和细胞外基质蛋白结合,并且在局部粘附形成中至关重要。然而,尚未研究其对压力过载引起的心力衰竭期间对冠状动脉血管生成的影响。在这里,我们假设Syndecan-4Modulates心脏重塑响应于压力过载,通过其调节适应性血管生成的能力。将Syndecan-4敲除(Syndecan-4 KO)和野生型(WT)小鼠受到横向主动脉收缩(TAC)诱导的压力过载。 Syndecan-4 KO小鼠表现出降低的毛细血管密度,减毒的心肌细胞尺寸,TAC手术后左心室心脏功能和WT小鼠的毛细血管功能。此外,Syndecan-4 KO小鼠显示出蛋白激酶Cα表达的显着降低。我们的数据表明,在压力过载后心力衰竭过程中,Syndecan-4对于补偿肥大和心功能的维护至关重要。 (c)2017年由elsevier公司发布

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