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|本期目录/Table of Contents|

钙化性主动脉瓣膜病的分子生物学机制及展望

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第3期
页码:
355-359
栏目:
综述
出版日期:
2018-03-25

文章信息/Info

Title:
Molecular biological mechanism of aortic calcification and prospect
作者:
程治源1; 宗刚军2
（1.安徽医科大学无锡临床学院心血管内科，江苏 无锡 214044；2.中国人民解放军第101医院心血管内科，江苏 无锡 214044）
Author(s):
CHENG Zhi-yuan1;  ZONG Gang-jun2
(1.Department of Cardiology, Wuxi Clinical Hospital, Anhui Medical University, Wuxi 214044, Jiangsu, China; 2.Department of Cardiology, PLA 101 Hospital, Wuxi 214044, Jiangsu, China)
关键词:
钙化性主动脉瓣膜病; 瓣膜间质细胞; 骨质疏松症; 分子生物学机制; 治疗
Keywords:
calcified aortic valve disease;  valve interstitial cells;  osteoporosis;  Mechanism of molecular biology;  treatment
分类号:
R542.5
DOI:
-
文献标识码:
A
摘要:
钙化性主动脉瓣膜病（CAVD）是中老年人最常见的心脏瓣膜病。随着人类寿命的增加，CAVD患病率预计将上升。三分之一老年人的超声心动图或X线检查发现主动脉瓣钙化的证据，是CAVD早期的亚临床形式。在全世界范围内，年龄、性别、吸烟、高胆固醇血症、高血压和II型糖尿病都是CAVD的危险因素。钙化性主动脉瓣狭窄是该病进展的最严重形式，而且有2%>60岁的人受到主动脉狭窄的影响，在一定程度上施行手术干预是必需的。在CAVD的临床进展的阶段没有有效的药物治疗。在最初阶段，发病机制类似于动脉粥样硬化，其特征是基底膜破裂，炎症反应、浸润、脂质沉积、钙化。骨桥蛋白在钙化主动脉瓣膜上的表达表明出现了病理性钙化，同时钙化瓣膜中有骨的形成。钙化的矿物质沉积在心血管软组织可破坏这些组织的正常生物力学功能，导致如心力衰竭、心肌梗死、中风并发症。本文重点阐述了CAVD分子和细胞水平的最新研究进展，并对未来的治疗方法进行了展望。
Abstract:
Calcific aortic valve disease (CAVD) is the most common valvular heart disease of the elderly. As life expectancy increases, prevalence of CAVD is expected to rise. One third of our elderly population has echocardiographic or radiological evidence of calcific aortic valve sclerosis, an early and subclinical form of CAVD. Age, gender, smoking, tobacco use, hypercholesterolemia, hypertension, and type II diabetes mellitus all contribute to the risk of the disease that has worldwide distribution. On progression to its most severe form, calcific aortic stenosis, CAVD can be devastating and 2% of the individuals >60 years are affected by calcific aortic stenosis to the extent that surgical intervention is required. No effective pharmacotherapies currently exist for treating those at risk for clinical progression. In the initial stages, the pathogenesis is similar to atherosclerosis, characterized by basement membrane disruption, inflammation, cell infiltration, lipid deposition, and calcification. Presence of osteopontin in calcified aortic valves suggests pathological calcification and bone formation in these calcified valves. Calcific mineral deposition within the soft cardiovascular tissues disrupts the normal biomechanical function of these tissues, leading to complications, including heart failure, myocardial infarction, and stroke. In this review, our investigation highlights current understanding of CAVD, emphasizing molecular and cellular aspects of its recent research and reviewing newer treatment strategies.

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备注/Memo

备注/Memo:
收稿日期：2016-12-02.基金项目：国家自然科学基金项目资助(81371657) 通讯作者：宗刚军，副主任医师，主要从事心脏瓣膜病基础与临床研究 Email:zonggj@163.com 作者简介：程治源，硕士生 Email:15205215338@163.com
更新日期/Last Update: 1900-01-01