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大骨节病软骨细胞发生坏死的分子生物学机制
引用本文:郭雄.大骨节病软骨细胞发生坏死的分子生物学机制[J].西安交通大学学报(医学版),2005,26(3):201-204.
作者姓名:郭雄
作者单位:西安交通大学教育部环境与疾病相关基因重点实验室,环境与地方病研究室,陕西西安,710061
基金项目:国家自然科学基金资助项目(No.30371252)
摘    要:目的综述大骨节病软骨细胞发生坏死的分子生物学研究进展。方法采用文献调查方法,对比分析国内外有关大骨节病与关节病的研究现状。结果大骨节病核心家庭有家庭聚集性趋势,患者软骨除表现有深层软骨细胞坏死外,还表现有软骨细胞过度凋亡和去分化;与骨关节病比较,大骨节病尚未开展STR多态性、软骨胶原基因和基因芯片方面的研究。结论应采用STR多态性、软骨胶原基因、基因芯片技术深入研究大骨节病分子生物学机制。

关 键 词:大骨节病  软骨细胞  基因  分子生物学
文章编号:1671-8259(2005)03-0201-04
修稿时间:2004年11月11

Molecular biological mechanism on chondronecrosis in cartilage with Kashin-Beck disease
GUO Xiong.Molecular biological mechanism on chondronecrosis in cartilage with Kashin-Beck disease[J].Journal of Xi‘an Jiaotong University:Medical Sciences,2005,26(3):201-204.
Authors:GUO Xiong
Abstract:Objective To review the progression of molecular biological mechanism on chondronecrosis in cartilage with Kashin-Beck disease (KBD) so as to promote the research work for pathogenesis of KBD. Methods The document analysis was used to compare the status quo of domestic and abroad research on KBD and osteoarthrosis. Results An aggregation in pedigrees with KBD was found, and an excessive chondrocyte apoptosis and de-differentiation was observed in cartilage from KBD patients except for chondronecrosis in deep zone. In contrast to osteoarthrosis, short tandem repeat, collagen gene in cartilage and gene chip were little known in KBD. Conclusion The pathogenesis of KBD should be further studied using modern biotechonology, such as short tandem repeat, cartilage collagen gene and gene chip.
Keywords:Kashin-Beck disease  chondrocyte  gene  molecular biology
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