Kyng Kasper J, Bohr Vilhelm A
Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
Ageing Res Rev. 2005 Nov;4(4):579-602. doi: 10.1016/j.arr.2005.06.008. Epub 2005 Oct 24.
Human progeroid syndromes are caused by mutations in single genes accelerating some but not all features of normal aging. Most progeroid disorders are linked to defects in genome maintenance, and while it remains unknown if similar processes underlie normal and premature aging, they provide useful models for the study of aging. Altered transcription is speculated to play a causative role in aging, and is involved in the pathology of most if not all progeroid syndromes. Previous studies demonstrate that there is a similar pattern of gene expression changes in primary cells from old and Werner syndrome compared to young suggesting a presence of common cellular aging mechanisms in old and progeria. Here we review the role of transcription in progeroid syndromes and discuss the implications of similar transcription aberrations in normal and premature aging.
人类早衰综合征是由单个基因突变引起的，这些突变加速了正常衰老的部分而非全部特征。大多数早衰症都与基因组维护缺陷有关，虽然正常衰老和早衰是否由相似过程导致仍不清楚，但它们为衰老研究提供了有用的模型。推测转录改变在衰老过程中起致病作用，并且涉及大多数（如果不是全部）早衰综合征的病理过程。先前的研究表明，与年轻细胞相比，老年细胞和沃纳综合征患者原代细胞中的基因表达变化模式相似，这表明老年和早衰存在共同的细胞衰老机制。在此，我们综述转录在早衰综合征中的作用，并讨论正常衰老和早衰中相似转录异常的影响。
