Cardiac LXR α protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization-Reference-Cited by-同舟云学术

Cardiac LXR α protects against pathological cardiac hypertrophy and dysfunction by enhancing glucose uptake and utilization

Published:2015-07-14 Issue:9 Volume:7 Page:1229-1243
ISSN:1757-4676
Container-title:EMBO Molecular Medicine
language:en
Short-container-title:EMBO Mol Med

Author:

Cannon Megan V¹,Silljé Herman HW¹,Sijbesma Jürgen WA²,Vreeswijk‐Baudoin Inge¹,Ciapaite Jolita³,van der Sluis Bart⁴,van Deursen Jan⁵,Silva Gustavo JJ⁶,de Windt Leon J⁶,Gustafsson Jan‐Åke⁷⁸,van der Harst Pim¹,van Gilst Wiek H¹,de Boer Rudolf A¹

Affiliation:

1. Department of Cardiology University Medical Center Groningen University of Groningen Groningen The Netherlands

2. Department of Nuclear Medicine University Medical Center Groningen University of Groningen Groningen The Netherlands

3. Department Pediatrics Center for Liver Digestive and Metabolic Diseases University Medical Center Groningen University of Groningen Groningen The Netherlands

4. Department of Pathology and Medical Biology University Medical Center Groningen University of Groningen Groningen The Netherlands

5. Department of Biochemistry & Molecular Biology Mayo Clinic Rochester MN USA

6. Department of Cardiology CARIM School for Cardiovascular Diseases Maastricht University Maastricht The Netherlands

7. Department of Biology and Biochemistry University of Houston Houston TX USA

8. Department of Biosciences and Nutrition Novum Karolinska Institutet Huddinge Sweden

Publisher

EMBO

Subject

Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/emmm.201404669

Reference56 articles.

1. Hepatic cholesterol metabolism and resistance to dietary cholesterol in LXRβ-deficient mice

2. Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts

3. Targeting myocardial substrate metabolism in heart failure: potential for new therapies

4. Liver X Receptor Signaling Is a Determinant of Stellate Cell Activation and Susceptibility to Fibrotic Liver Disease

5. Assessing mitochondrial dysfunction in cells

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