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马凡综合征:基因型-表型相关性的新线索

Marfan syndrome: new clues to genotype-phenotype correlations.

作者信息

Ramirez F, Gayraud B, Pereira L

机构信息

Department of Biochemistry and Molecular Biology, Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

Ann Med. 1999 Jun;31(3):202-7. doi: 10.3109/07853899909115979.

Abstract

Fibrillin 1 is the main constituent of extracellular microfibrils. Microfibrils can exist as individual structures or associate with elastin to form elastic fibres. Fibrillin 1 mutations are the cause of the pleiotropic manifestations of the Marfan syndrome (MFS) which principally involve the musculoskeletal, ocular and cardiovascular systems. MFS pathogenesis requires high levels of mutant fibrillin 1 molecules with dominant-negative activity on microfibrillar assembly and function. Gene-targeting experiments in the mouse have shed new light on fibrillin 1 function, genotype-phenotype correlations and aneurysm progression. These experiments have documented the involvement of fibrillin 1 in maintaining tissue homeostasis, suggested the existence of a critical threshold of functional microfibrils for tissue biomechanics, and outlined novel contributors to the pathogenic sequence of vascular wall collapse.

摘要

原纤蛋白1是细胞外微原纤维的主要成分。微原纤维可以作为独立结构存在,也可以与弹性蛋白结合形成弹性纤维。原纤蛋白1突变是马凡综合征(MFS)多效性表现的原因,主要累及肌肉骨骼、眼部和心血管系统。MFS发病机制需要高水平具有对微原纤维组装和功能起显性负性作用的突变原纤蛋白1分子。小鼠基因靶向实验为原纤蛋白1功能、基因型-表型相关性及动脉瘤进展提供了新线索。这些实验证明了原纤蛋白1在维持组织稳态中的作用,提示了组织生物力学中功能性微原纤维临界阈值的存在,并概述了血管壁塌陷致病序列的新因素。

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