Novartis Professor of Biology, Director of the Glenn Labs for the Science of Aging, and Affiliate of the Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 02139, USA.
Cell Metab. 2014 Nov 4;20(5):706-707. doi: 10.1016/j.cmet.2014.10.015.
Diseases due to DNA damage repair machinery defects can resemble premature aging. In this issue of Cell Metabolism, Scheibye-Knudsen et al. (2014) demonstrate that increasing NAD(+) levels may reverse the inactivation of Sirt1 and mitochondrial defects in Cockayne Syndrome B that stem from nuclear NAD(+) depletion by the DNA repair protein PARP.
由于 DNA 损伤修复机制缺陷导致的疾病可能类似于早衰。在本期《细胞代谢》中,Scheibye-Knudsen 等人(2014)表明,增加 NAD(+)水平可能逆转 Cockayne 综合征 B 中 Sirt1 的失活和线粒体缺陷,这是由于 DNA 修复蛋白 PARP 导致核 NAD(+)耗竭引起的。