Diabetes and Cardiovascular Research Center, University of Missouri School of Medicine, D109 Diabetes Center HSC, One Hospital Drive, Columbia, MO, 65212, USA.
Research Service, Truman Memorial Veterans Hospital, Columbia, MO, 65201, USA.
Curr Hypertens Rep. 2018 Jul 6;20(9):76. doi: 10.1007/s11906-018-0876-9.
Increased arterial stiffness, an abnormal structural and functional change in the vascular wall, is a precursor for hypertension, coronary heart disease, stroke, and associated cardiovascular disease (CVD). The aim of this paper is to review the etiology of arterial stiffening and potential therapeutic approaches to modulate arterial fibrosis and stiffness.
The Framingham Heart Study demonstrated that arterial stiffness is an independent predictor of CVD and related morbidity and mortality. Dysfunction of endothelial cells, vascular smooth muscle cells, extracellular matrix, and other functional elements of the vessel wall contribute to underlying pathophysiology of increased arterial stiffness. An activated renin-angiotensin-aldosterone system, oxidative stress, abnormal peri-vascular adipose tissue, inflammation, and increased sympathetic nervous system activity are associated with the development and progression of arterial fibrosis, stiffening, and associated CVD. In this review, we will discuss the structural and function changes and mechanisms of the vessel wall in arterial stiffness and provide potential therapeutic strategies.
动脉僵硬度增加是血管壁结构和功能的异常改变，是高血压、冠心病、卒中和相关心血管疾病（CVD）的先兆。本文旨在综述动脉僵硬度的病因学以及调节动脉纤维化和僵硬度的潜在治疗方法。
弗雷明汉心脏研究表明，动脉僵硬度是 CVD 及其相关发病率和死亡率的独立预测因子。内皮细胞、血管平滑肌细胞、细胞外基质和血管壁的其他功能元素的功能障碍导致动脉僵硬度增加的潜在病理生理学。激活的肾素-血管紧张素-醛固酮系统、氧化应激、异常的血管周围脂肪组织、炎症和增加的交感神经系统活动与动脉纤维化、僵硬度和相关 CVD 的发展和进展有关。在本综述中，我们将讨论血管壁在动脉僵硬度中的结构和功能变化及其机制，并提供潜在的治疗策略。
