Large arteries (especially the aorta) lose elasticity and thicken with aging and as a consequence of other conditions, thus leading to central arterial stiffening and associated adverse effects on blood flow and pressure. Arterial stiffness can be defined and measured in different ways, at a local level or systemically. Increases in either the intrinsic (material) stiffness or net structural (combined geometric and material) arterial stiffness, or both, can increase the velocity at which the pressure pulse travels along the arterial tree and central pulse pressure, which can negatively impact downstream resistance vessels and organs (ie, heart, brain, and kidney). Clarifying temporal and causal relationships between arterial stiffening and hypertension was identified by NHLBI as an important gap of knowledge, with a potential for clinical translation. NIH (National Institutes of Health)-funded studies, more than half of them supported by the NHLBI (Online Figure), have investigated various aspects of arterial stiffening in humans and in experimental models. To enable a more focused research effort on this topic, NHLBI launched a Request for Applications (RFA) HL-10 -027, entitled Cellular and Molecular Mechanisms of Arterial Stiffening and Its Relationship to Development of Hypertension (R01). This initiative supported 11 R01 awards during 2010 to 2015 (Online Table II; cumulative ≈ $20 million dollars in total costs), which represented a significant component of the overall NHLBI investment in this field. Here, we report a summary of important scientific findings that resulted from this NHLBI-initiated research effort, constituting the basis of > 200 original research and review articles (Online Table II), some highlighted here, many conference presentations, and several patents . In humans, increased arterial stiffness, or loss of elastic compliance of large arteries, has been linked to an increased risk of myocardial infarction, heart failure, stroke, and kidney disease, among other conditions. Pulse wave velocity (PWV), …

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关于NHLBI研究动脉僵硬及其与高血压关系的细胞和分子机制的倡议的特别报告

大动脉（尤其是主动脉）会随着年龄的增长以及其他情况而失去弹性并增厚，从而导致中央动脉硬化以及对血流和压力的不利影响。可以以不同的方式在局部水平或系统地定义和测量动脉僵硬度。固有（材料）刚度或净结构（几何和材料组合）动脉刚度或两者的增加，可能会增加压力脉冲沿动脉树传播的速度和中心脉冲压力，这可能会对下游阻力血管产生负面影响和器官（即心脏，大脑和肾脏）。NHLBI认为，弄清动脉硬化与高血压之间的时间和因果关系是重要的知识缺口，具有临床翻译的潜力。由美国国立卫生研究院（NIH）资助的研究，其中超过一半由NHLBI（在线图）支持，已经研究了人体和实验模型中动脉硬化的各个方面。为了使对该主题的研究更加集中，NHLBI发起了一项名为HL-10 -027的申请书，标题为“动脉硬化的细胞和分子机制及其与高血压发展的关系（R01）”。该倡议支持了2010年至2015年的11个R01奖励（在线表II；累计总成本≈2000万美元），占NHLBI在该领域投资总额的重要组成部分。在这里，我们总结了由NHLBI发起的研究工作所产生的重要科学发现的摘要，构成了> 200篇原始研究和评论文章（在线表II），此处突出显示，许多会议介绍以及多项专利。在人类中，动脉僵硬度增加或大动脉弹性顺应性下降与心肌梗塞，心力衰竭，中风和肾脏疾病等其他疾病的风险增加有关。脉搏波速度（PWV），…