2017年6月
Hypercholesterolemia Causes Circadian Dysfunction: A Potential Risk Factor for Cardiovascular Disease
EBioMedicine
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- 巻
- 20
- 号
- 開始ページ
- 127
- 終了ページ
- 136
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.ebiom.2017.04.034
- 出版者・発行元
- ELSEVIER SCIENCE BV
Hypercholesterolemia is a well-known risk factor for a wide range of diseases in developed countries. Here, we report that mice lacking functional LDLR (low density lipoprotein receptor), an animal model of human familial hypercholesterolemia, show circadian abnormalities. In free running behavioral experiments in constant darkness, these mice showed a prolonged active phase and distinctly bimodal rhythms. Even when the circadian rhythms were entrained by light and dark cycles, these mice showed a significant attenuation of behavioral onset intensity at the start of the dark period. Further, we hypothesized that the combination of hypercholesterolemia and circadian abnormalities may affect cardiovascular disease progression. To examine this possibility, we generated LDLR-deficient mice with impaired circadian rhythms by simultaneously introducing a mutation into Period2, a core clock gene, and found that these mice showed a significant enlargement of artery plaque area with an increase in inflammatory cytokine IL-6 levels. These results suggest that circadian dysfunction may be associated with the development or progression of cardiovascular diseases. (C) 2017 The Authors. Published by Elsevier B.V.
- リンク情報
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- DOI
- https://doi.org/10.1016/j.ebiom.2017.04.034
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/28499924
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000405719700020&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85019056127&origin=inward 本文へのリンクあり
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85019056127&origin=inward
- ID情報
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- DOI : 10.1016/j.ebiom.2017.04.034
- ISSN : 2352-3964
- eISSN : 2352-3964
- PubMed ID : 28499924
- SCOPUS ID : 85019056127
- Web of Science ID : WOS:000405719700020