Durieux Jenni, Dillin Andrew
Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
Cell Metab. 2007 Dec;6(6):427-9. doi: 10.1016/j.cmet.2007.11.008.
Metabolic component depletion in model systems results in life-span extension, which has been difficult to reconcile with human metabolic pathologies. Recently, Rea et al. (2007) have shown that mitochondrial electron transport chain RNAi phenotypes in the worm C. elegans are dose dependent, providing an alternative view of mitochondrial function in longevity and metabolic diseases.
模型系统中的代谢成分耗竭会导致寿命延长,这一直难以与人类代谢病理学相协调。最近,雷亚等人(2007年)表明,线虫秀丽隐杆线虫中线粒体电子传递链RNA干扰表型是剂量依赖性的,这为线粒体功能在长寿和代谢疾病中的作用提供了另一种观点。