JCL roundtable: Lipids and inflammation in atherosclerosis |
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Authors: | Karin E Bornfeldt MacRae F Linton Edward A Fisher John R Guyton |
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Affiliation: | 1. University of Washington Medicine Diabetes Institute, Division of Metabolism, Endocrinology and Nutrition, Departments of Medicine and Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA;2. Lipid Clinic and Atherosclerosis Research Unit, Division of Cardiovascular Medicine, Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, TN, USA;3. Division of Cardiology, Center for the Prevention of Cardiovascular Disease, Cardiovascular Research Center, New York University Grossman School of Medicine, New York, NY, USA;4. Division of Endocrinology, Metabolism, and Nutrition, Department of Medicine, Duke University Medical Center, Durham, NC, USA |
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Abstract: | Clinical effort in lipidology focuses largely on mitigating effects of atherosclerosis, a pathologic process localized to the intimal layer of larger arteries. This JCL Roundtable brings together 3 leading researchers to discuss the current understanding of pathogenesis in atherosclerosis. We begin by recognizing that low density lipoprotein concentrations in arterial intima far exceed concentrations in other connective tissues, consistent with the response-to-retention hypothesis of atherogenesis. High density lipoproteins facilitate reverse cholesterol transport and also have antioxidant and anti-inflammatory roles. New evidence points to remnants of triglyceride-rich lipoproteins as promoters of atherogenesis, highlighted by deleterious effects of apolipoprotein C-III. The multifaceted role of inflammation is becoming clearer through discoveries related to leukocyte recruitment, efferocytosis, resolution of inflammation, and crystal formation. MicroRNAs represent a new, complex mode of gene regulation bearing on lipoprotein and inflammation biology. Progress in understanding atherosclerosis portends a future in which residual risk related to obesity, diabetes, and other factors will yield to new targeted therapies. |
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Keywords: | atherosclerosis lipoproteins response-to-retention hypothesis inflammation resolution of inflammation efferocytosis microRNAs |
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