Cellular and molecular mechanisms of thoracic aortic aneurysms

被引:261
作者
El-Hamamsy, Ismail [1 ]
Yacoub, Magdi H. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Harefield Heart Sci Ctr, Magdi Yacoub Inst, London, England
关键词
GROWTH-FACTOR-BETA; SMOOTH-MUSCLE-CELLS; PATENT DUCTUS-ARTERIOSUS; MARFAN-SYNDROME; MATRIX METALLOPROTEINASES; MOUSE MODEL; CANINE ATHEROSCLEROSIS; EXTRACELLULAR-MATRIX; SIGNALING PATHWAYS; MISSENSE MUTATION;
D O I
10.1038/nrcardio.2009.191
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Thoracic aortic aneurysms (TAA) increase the risk of aortic dissection or rupture and represent an important source of morbidity and mortality. Inherited forms of the disease, including Marfan syndrome, have been recognized for a long time but were considered degenerative diseases characterized by cystic medial necrosis of the aortic wall. Improved definition of the structure and function of the normal aortic wall, coupled with the discovery of genetic mutations in key regulatory molecules, have contributed to a more detailed understanding of the pathophysiology of syndromic, familial and sporadic TAAs. We here review the cellular and molecular mechanisms involved in TAA formation and outline areas for future research.
引用
收藏
页码:771 / 786
页数:16
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