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红细胞膜疾病

Disorders of red cell membrane.

作者信息

An Xiuli, Mohandas Narla

机构信息

Red Cell Physiology Laboratory, New York Blood Center, New York, NY 10065, USA.

出版信息

Br J Haematol. 2008 May;141(3):367-75. doi: 10.1111/j.1365-2141.2008.07091.x. Epub 2008 Mar 12.

Abstract

Studies during the last three decades have enabled the development of detailed molecular insights into the structural basis of altered function in various inherited red cell membrane disorders. This review highlights our current understanding of molecular and mechanistic insights into various inherited red cell membrane disorders involving either altered membrane structural organization (hereditary spherocytosis, hereditary elliptocytosis and hereditary ovalocytosis) or altered membrane transport function (hereditary stomatocytosis). The molecular basis for the vast majority of cases of hereditary spherocytosis, elliptocytosis and ovalocytosis have been fully defined while little progress has been made in defining the molecular basis for hereditary stomatocytosis. Mutations in a number of distinct genes account for hereditary spherocytosis and elliptocytosis, while a single genetic defect accounts for all cases of hereditary ovalocytosis. Based on these molecular insights, a comprehensive understanding of the structural basis for altered membrane function has been developed. Loss of vertical linkage between membrane skeleton and lipid bilayer leads to membrane loss in hereditary spherocytosis, while weakening of lateral linkages between skeletal proteins leads to membrane fragmentation and surface area loss in hereditary elliptocytosis. Importantly, the severity of anaemia in both these disorders is directly related to extent of membrane surface area loss. Splenectomy results in amelioration of anaemia.

摘要

过去三十年的研究使得人们能够深入了解各种遗传性红细胞膜疾病功能改变的结构基础的详细分子机制。本综述着重介绍了我们目前对各种遗传性红细胞膜疾病的分子和机制的理解,这些疾病包括膜结构组织改变(遗传性球形红细胞增多症、遗传性椭圆形红细胞增多症和遗传性卵形红细胞增多症)或膜转运功能改变(遗传性口形红细胞增多症)。绝大多数遗传性球形红细胞增多症、椭圆形红细胞增多症和卵形红细胞增多症病例的分子基础已得到充分明确,而在确定遗传性口形红细胞增多症的分子基础方面进展甚微。许多不同基因的突变导致遗传性球形红细胞增多症和椭圆形红细胞增多症,而单一的基因缺陷则导致所有遗传性卵形红细胞增多症病例。基于这些分子见解,人们对膜功能改变的结构基础有了全面的认识。膜骨架与脂质双层之间垂直连接的丧失导致遗传性球形红细胞增多症中的膜丢失,而骨架蛋白之间横向连接的减弱导致遗传性椭圆形红细胞增多症中的膜碎片化和表面积丢失。重要的是,这两种疾病中贫血的严重程度与膜表面积丢失的程度直接相关。脾切除可改善贫血症状。

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