Rodríguez Sofía, Eriksson Maria
Department of Biosciences and Nutrition, Karolinska Institutet, Karolinska University Hospital, Huddinge, Stockholm, Sweden.
Curr Aging Sci. 2010 Jul;3(2):81-9. doi: 10.2174/1874609811003020081.
The molecular mechanisms that cause physiological aging are still not completely understood, most likely because of the complex nature of the aging process. Recent discoveries on segmental progeroid syndromes emphasize the importance of studying rare diseases to discover more common mechanisms. Since the identification of mutations in the LMNA gene that causes the segmental progeroid syndrome, Hutchinson-Gilford progeria syndrome (HGPS), there has been an increasing interest in the potential role for lamins in the normal aging process. Recent data provide support for the shared mechanisms between natural and pathological aging, and show that further studies of HGPS and segmental progeroid syndromes will be of use in solving the aging puzzle. In this review, we summarize the recent findings and discuss the existing evidence for an important functional link between lamins and the aging process. In addition, we discuss the evidence for a mechanism in which defects in lamins result in genomic instability and senescence.
导致生理性衰老的分子机制仍未完全明确，这很可能是由于衰老过程的复杂性所致。近期关于节段性早衰综合征的发现强调了研究罕见病以发现更常见机制的重要性。自从鉴定出导致节段性早衰综合征——哈钦森 - 吉尔福德早衰综合征（HGPS）的LMNA基因突变以来，人们对核纤层蛋白在正常衰老过程中的潜在作用越来越感兴趣。最新数据为自然衰老和病理性衰老之间的共同机制提供了支持，并表明对HGPS和节段性早衰综合征的进一步研究将有助于解开衰老之谜。在本综述中，我们总结了近期的研究结果，并讨论了核纤层蛋白与衰老过程之间重要功能联系的现有证据。此外，我们还讨论了核纤层蛋白缺陷导致基因组不稳定和衰老的机制证据。
