Aortic stiffness and polymorphisms of collagen-1 type 1a gene in COPD patients

T. Brodskaya, V. Nevzorova, N. Zakharchuk, N. Repina
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引用次数: 2

Abstract

Currently the connection between chronic obstructive respiratory disease COPD and some cardiovascular and cerebrovascular diseases has been established Vascular disorders in COPD become evident in the early stages of disease and can manifest from endothelial dysfunction to aortic mechanical property disturbance and cerebral circulation disorders COPD is also known as a disease associated with smoking A number of researchers have described pathophysiological mechanisms of vascular disorders and in particular arterial stiffening in COPD A variety of theories have been proposed to explain these observations Pathophysiological processes that increase arterial stiffness both physiological and pathophysiological involve remodeling cascades leading to disturbance of the structural and functional relationships between collagen and elastin in the arterial vascular wall The main processes involved appear to be inflammatory proteases and oxidative stress New research suggests that the vascular dysfunction observed in COPD is associated with some specific genes New data suggests that this is not just due to endothelial dysfunction but a violation of the mechanical properties of the arterial vasculature which is now considered an important component of the pathogenesis of COPD Surplus aortic stiffness can contribute increasingly to cardiovascular event risk in COPD and is associated with changes in normal cerebral circulation and cognitive function Research is focused on the study of genetic predisposition for vascular dysfunction in COPD Various polymorphisms determining the connective tissue metabolism production of nitric oxide detoxification of xenobiotics and many others are now all thought relevant Increasing of aortic stiffness is an important component of the amplification of cardiovascular risk events coronary disorders and cerebral circulation in patients with COPD Some polymorphisms are considered especially relevant such as COL A polymorphisms It is now important to take into consideration the pathophysiological consequences of increasing arterial stiffness in COPD which are schematically represented in our review
COPD患者主动脉硬化与胶原-1 1a型基因多态性
目前慢性阻塞性呼吸系统疾病COPD与一些心脑血管疾病之间的联系已经确立,COPD的血管障碍在疾病早期就很明显,可以表现为内皮功能障碍、主动脉力学性能障碍和脑循环障碍,COPD也被称为与吸烟相关的疾病,许多研究者已经描述了血管障碍的病理生理机制和人们提出了多种理论来解释这些观察结果,增加动脉僵硬的病理生理过程包括生理和病理生理上的重塑级联反应,导致动脉血管壁中胶原蛋白和弹性蛋白之间的结构和功能关系受到干扰,主要过程似乎是炎症蛋白酶和氧化应激新的数据表明,这不仅仅是由于内皮功能障碍,而且是动脉血管力学特性的破坏,这被认为是慢性阻塞性肺病发病机制的重要组成部分,主动脉僵硬过剩可以增加慢性阻塞性肺病心血管事件的风险,并与正常脑循环和认知功能的改变有关慢性阻塞性肺病血管功能障碍的遗传易感性决定结缔组织代谢、一氧化氮产生、外源药物解毒和许多其他因素的各种多态性现在都被认为与之相关。主动脉僵硬度增加是慢性阻塞性肺病患者心血管危险事件增加的重要组成部分冠状动脉疾病和脑循环。一些多态性被认为特别相关,如cola多态性考虑到慢性阻塞性肺病中动脉僵硬度增加的病理生理后果,这在我们的综述中有图示
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