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Atherosclerosis: current pathogenesis and therapeutic options

Coronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of li... Full description

Journal Title: Nature medicine 2011-11, Vol.17 (11), p.1410-1422
Main Author: Weber, Christian
Other Authors: Noels, Heidi
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Nature Publishing Group
ID: ISSN: 1078-8956
Link: https://www.ncbi.nlm.nih.gov/pubmed/22064431
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title: Atherosclerosis: current pathogenesis and therapeutic options
format: Article
creator:
  • Weber, Christian
  • Noels, Heidi
subjects:
  • Adaptive Immunity
  • Atherosclerosis
  • Atherosclerosis - complications
  • Atherosclerosis - drug therapy
  • Atherosclerosis - pathology
  • Atherosclerosis - physiopathology
  • B-Lymphocytes - immunology
  • Care and treatment
  • Causes of
  • Chemokines - immunology
  • Coronary Artery Disease - drug therapy
  • Coronary Artery Disease - etiology
  • Coronary Artery Disease - pathology
  • Coronary Artery Disease - physiopathology
  • Dendritic Cells - immunology
  • Development and progression
  • Diagnosis
  • Drug therapy
  • Genetics
  • Homeostasis
  • Humans
  • Immunity, Innate
  • Inflammation - pathology
  • Inflammation - physiopathology
  • Lipid Metabolism
  • Lipids
  • Neutrophils - physiology
  • Pathology
  • Pharmacology
  • Receptors, Chemokine - immunology
  • T-Lymphocytes - immunology
ispartof: Nature medicine, 2011-11, Vol.17 (11), p.1410-1422
description: Coronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.
language: eng
source:
identifier: ISSN: 1078-8956
fulltext: no_fulltext
issn:
  • 1078-8956
  • 1546-170X
url: Link


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descriptionCoronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.
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subjectAdaptive Immunity ; Atherosclerosis ; Atherosclerosis - complications ; Atherosclerosis - drug therapy ; Atherosclerosis - pathology ; Atherosclerosis - physiopathology ; B-Lymphocytes - immunology ; Care and treatment ; Causes of ; Chemokines - immunology ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - etiology ; Coronary Artery Disease - pathology ; Coronary Artery Disease - physiopathology ; Dendritic Cells - immunology ; Development and progression ; Diagnosis ; Drug therapy ; Genetics ; Homeostasis ; Humans ; Immunity, Innate ; Inflammation - pathology ; Inflammation - physiopathology ; Lipid Metabolism ; Lipids ; Neutrophils - physiology ; Pathology ; Pharmacology ; Receptors, Chemokine - immunology ; T-Lymphocytes - immunology
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abstractCoronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.
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