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The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Journal article
Authors Jeanna Perman
Pontus Boström
Malin Lindbom
Ulf Lidberg
Marcus Ståhlman
Daniel Hägg
Henrik Lindskog
Margareta Scharin Täng
Elmir Omerovic
Lillemor Mattsson Hultén
Anders Jeppsson
Petur Petursson
Johan Herlitz
Gunilla Olivecrona
Dudley K Strickland
Kim Ekroos
Sven-Olof Olofsson
Jan Borén
Published in The Journal of clinical investigation
Volume 121
Issue 7
Pages 2625-40
ISSN 1558-8238
Publication year 2011
Published at Wallenberg Laboratory
Institute of Medicine
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 2625-40
Language en
Keywords Animals, Apoptosis, physiology, Cell Line, Endoplasmic Reticulum, metabolism, Humans, Lipid Metabolism, Lipids, chemistry, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocardial Infarction, mortality, pathology, physiopathology, Myocardial Ischemia, mortality, pathology, physiopathology, Myocardium, cytology, metabolism, pathology, Receptors, LDL, genetics, metabolism, Stress, Physiological, Survival Rate, Triglycerides, toxicity
Subject categories Medical and Health Sciences


Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr-/- mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr-/- mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.

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