Li Baomin, Jog Sonali, Candelario Jose, Reddy Sita, Comai Lucio
Department of Molecular Microbiology and Immunology, Institute for Genetic Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.
ScientificWorldJournal. 2009 Dec 16;9:1449-62. doi: 10.1100/tsw.2009.159.
Syndromes of accelerated aging could provide an entry point for identifying and dissecting the cellular pathways that are involved in the development of age-related pathologies in the general population. However, their usefulness for aging research has been controversial, as it has been argued that these diseases do not faithfully reflect the process of natural aging. Here we review recent findings on the molecular basis of two progeroid diseases, Werner syndrome (WS) and Hutchinson-Gilford progeria syndrome (HGPS), and highlight functional connections to cellular processes that may contribute to normal aging.
加速衰老综合征可能为识别和剖析普通人群中与年龄相关病理发展所涉及的细胞途径提供切入点。然而,它们在衰老研究中的有用性一直存在争议,因为有人认为这些疾病并不能如实地反映自然衰老过程。在这里,我们回顾了关于两种早老性疾病——沃纳综合征(WS)和哈钦森 - 吉尔福德早衰综合征(HGPS)——分子基础的最新发现,并强调了与可能导致正常衰老的细胞过程的功能联系。