Genetics of aging, progeria and lamin disorders

被引:43
|
作者
Ghosh, Shrestha [1 ]
Zhou, Zhongjun [1 ,2 ]
机构
[1] Univ Hong Kong, Li Ka Shing Fac Med, Dept Biochem, Hong Kong, Hong Kong, Peoples R China
[2] Univ Hong Kong, Shenzhen Inst Res & Innovat, Shenzhen, Peoples R China
基金
中国国家自然科学基金;
关键词
HUTCHINSON-GILFORD-PROGERIA; DNA-REPAIR; TELOMERE LENGTH; GENOMIC INSTABILITY; DISEASE; ACCUMULATION; MAINTENANCE; DYSFUNCTION; MECHANISMS; SENESCENCE;
D O I
10.1016/j.gde.2014.05.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Premature aging disorders, like Werner syndrome, Bloom's syndrome, and Hutchinson-Gilford Progeria Syndrome (HOPS), have been the subjects of immense interest as they recapitulate many of the phenotypes observed in physiological aging. They, therefore, not only provide model systems to study normal aging processes but also give valuable insights into the intricate mechanisms underlying senescence. Recent works on HOPS have revealed alterations in a spectrum of cellular and molecular pathways involved in the maintenance of genomic integrity, thus suggesting a profound impact of the nuclear lamina in nuclear organization, chromatin dynamics, regulation of gene expression and epigenetics.
引用
收藏
页码:41 / 46
页数:6
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