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Rip2 deficiency leads to increased atherosclerosis despite decreased inflammation.

Journal article
Authors Malin Levin
Pernilla Jirholt
Anna Wramstedt
Maria E Johansson
Anna M Lundberg
Maria Gustafsson Trajkovska
Marcus Ståhlman
Per Fogelstrand
Mikael Brisslert
Linda Fogelstrand
Zhong-Qun Yan
Göran K Hansson
Harry Björkbacka
Sven-Olof Olofsson
Jan Borén
Published in Circulation research
Volume 109
Issue 11
Pages 1210-8
ISSN 1524-4571
Publication year 2011
Published at Wallenberg Laboratory
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 1210-8
Language en
Keywords Animals, Apolipoprotein B-100, genetics, Atherosclerosis, enzymology, etiology, immunology, pathology, Bone Marrow Transplantation, Cholesterol, metabolism, Humans, Inflammation, Lipoproteins, LDL, metabolism, Macrophages, Peritoneal, enzymology, physiology, Mice, Mice, Knockout, Mice, Transgenic, Pinocytosis, RNA, Messenger, biosynthesis, Radiation Chimera, Receptor-Interacting Protein Serine-Threonine Kinases, deficiency, genetics, immunology, Receptors, LDL, deficiency, genetics, Specific Pathogen-Free Organisms, Toll-Like Receptor 4, physiology, Triglycerides, metabolism
Subject categories Physiology


The innate immune system and in particular the pattern-recognition receptors Toll-like receptors have recently been linked to atherosclerosis. Consequently, inhibition of various signaling molecules downstream of the Toll-like receptors has been tested as a strategy to prevent progression of atherosclerosis. Receptor-interacting protein 2 (Rip2) is a serine/threonine kinase that is involved in multiple nuclear factor-κB (NFκB) activation pathways, including Toll-like receptors, and is therefore an interesting potential target for pharmaceutical intervention.

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