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Letter to the editor: 'Looking for molecular mechanisms underlying aberrant elastin deposition in hypertension'

机译:给编辑的信:“寻找高血压中异常弹性蛋白沉积的分子机制”

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to the editor: Elastic fibers may be key elements in the pathophysiology of hypertensive vascular remodeling. In addition to the well-known adverse effects of hypertension on the elastic fiber system, recent studies indicate that aberrant elastin deposition may precede the development of hypertension. In the December 2008 issue of American Journal of Physiology-Heart and Circulatory Physiology, Arribas and cowork-ers (1) demonstrated the deposition of excessive and aberrant elastin before the development of systemic hypertension in spontaneously hypertensive rats (SHRs). In neonatal SHRs, the isolated elastin scaffold of the aorta exhibited an increased relative weight and stiffness, as well as the presence of peculiar trabeculae inside the fenestrae that reduced their size. The authors concluded from their data that the aberrant elastin deposited in the SHR aorta alters the mechanical properties leading to compromised vessel expansion, compromised he-modynamic function, and finally to the development of hypertension. Since the abnormal organization does not occur in nongenetic models of hypertension, the authors speculate that a unique genetic program of SHRs triggers an early aberrant assembly of elastic lamellae and/or a lack of normal elastin remodeling.
机译:对于编辑:弹性纤维可以是高血压血管重塑病理生理学中的关键要素。除了众所周知的高血压对弹性纤维系统的不良反应外,最近的研究表明,异常的弹性蛋白沉积可在高血压的发育之前。 2008年12月,美国的生理学 - 心脏和循环生理学杂志,Arribas和Cowork-ers(1)展示了在自发性高血压大鼠(SHRS)的全身高血压发展之前沉积过量和异常的弹性蛋白。在新生儿SHRS中,主动脉的分离的弹性蛋白支架表现出相对重量和刚度的增加,以及在减少其尺寸的雪最低的特殊组成的存在。作者从他们的数据结束,即在SHR主动脉沉积在SHR主动脉中的异常弹性蛋白改变机械性能,导致血管膨胀的损伤,受损的HE-Mocynamic功能损害,并且最终发生高血压的发展。由于异常组织在高血压的环境模型中,作者推测,SCR的独特遗传程序触发了弹性薄片的早期异常组装和/或缺乏正常的弹性蛋白重塑。

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