期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2019
卷号：116
期号：27
页码：13171-13172
DOI：10.1073/pnas.1907751116
出版社：The National Academy of Sciences of the United States of America
摘要：How the mammalian circadian clock interacts with metabolism and its possible implications in metabolic diseases are actively studied. In PNAS, Foteinou et al. (1) propose a mathematical model of the circadian clock that incorporates the metabolic sensor SIRT1 and validate it with cell experiments. Their findings shed light on conflicting reports by Asher et al. (2) and Nakahata et al. (3) about the effect of SIRT1 deficiency on clock function and SIRT1 targets. Foteinou et al. (1) conclude that SIRT1 acts on the clock not only via the well-known clock protein PER2, but also through PGC1α, a transcriptional coactivator of the BMAL1 clock gene with key metabolic functions. Interestingly, the Foteinou et al. … [↵][1]2To whom correspondence may be addressed.
