Thalidomide-induced teratogenesis: History and mechanisms

被引:584
作者
Vargesson, Neil [1 ]
机构
[1] Univ Aberdeen, Inst Med Sci, Sch Med Sci, Aberdeen, Scotland
基金
英国惠康基金;
关键词
angiogenesis; reactive oxygen species; cell death; cereblon; actin cytoskeleton; limb development; Fgf8; Shh; phocomelia; vascular transition; GENE-EXPRESSION; LIMB DEFORMITIES; ROBERTS-SYNDROME; ANGIOGENESIS; EMBRYOPATHY; DEFECTS; MALFORMATIONS; ABNORMALITIES; HYPOTHESIS; EXPOSURE;
D O I
10.1002/bdrc.21096
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Nearly 60 years ago thalidomide was prescribed to treat morning sickness in pregnant women. What followed was the biggest man-made medical disaster ever, where over 10,000 children were born with a range of severe and debilitating malformations. Despite this, the drug is now used successfully to treat a range of adult conditions, including multiple myeloma and complications of leprosy. Tragically, a new generation of thalidomide damaged children has been identified in Brazil. Yet, how thalidomide caused its devastating effects in the forming embryo remains unclear. However, studies in the past few years have greatly enhanced our understanding of the molecular mechanisms the drug. This review will look at the history of the drug, and the range and type of damage the drug caused, and outline the mechanisms of action the drug uses including recent molecular advances and new findings. Some of the remaining challenges facing thalidomide biologists are also discussed. Birth Defects Research (Part C) 105:140-156, 2015. (c) 2015 Wiley Periodicals, Inc.
引用
收藏
页码:140 / 156
页数:17
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