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Treatment of calcified coronary lesions with Palmaz-Schatz stents. An intravascular ultrasound study Characteristics of abnormal post-stent optical coherence tomography findings in hemodialysis patients Coronary Microcirculation Downstream Non-Infarct-Related Arteries in the Subacute Phase of Myocardial Infarction: Implications for Physiology-Guided Revascularization Comparative efficacy of two paclitaxel-coated balloons with different excipient coatings in patients with coronary in-stent restenosis: A pooled analysis of the Intracoronary Stenting and Angiographic Results: Optimizing Treatment of Drug Eluting Stent In-Stent Restenosis 3 and 4 trials Cardiotoxicity and Cardiac Monitoring Among Chemotherapy-Treated Breast Cancer Patients Optical coherence tomography predictors of target vessel myocardial infarction after provisional stenting in patients with coronary bifurcation disease Lesion-Specific and Vessel-Related Determinants of Fractional Flow Reserve Beyond Coronary Artery Stenosis Anatomical and Functional Computed Tomography for Diagnosing Hemodynamically Significant Coronary Artery Disease: A Meta-Analysis Updated clinical classification of pulmonary hypertension Immunotherapy of Endothelin-1 Receptor Type A for Pulmonary Arterial Hypertension

Review ArticleVolume 74, Issue 12, September 2019

JOURNAL:J Am Coll Cardiol. Article Link

From Focal Lipid Storage to Systemic Inflammation

P Libby, GK Hansson. Keywords: inflammation; LDL cholesterol; smooth muscle cell

ABSTRACT


Concepts of atherogenesis have evolved considerably with time. Early animal experiments showed that a cholesterol-rich diet could induce fatty lesion formation in arteries. The elucidation of lipoprotein metabolism ultimately led to demonstrating the clinical benefits of lipid lowering. The view of atheromata as bland accumulations of smooth muscle cells that elaborated an extracellular matrix that could entrap lipids then expanded to embrace inflammation as providing pathways that could link risk factors to atherogenesis. The characterization of leukocyte adhesion molecules and their control by proinflammatory cytokines, the ability of chemokines to recruit leukocytes, and the identification of inflammatory cell subtypes in lesions spurred the unraveling of innate and adaptive immune pathways that contribute to atherosclerosis and its thrombotic complications. Such pathophysiologic insights have led to the identification of biomarkers that can define categories of risk and direct therapies and to the development of new treatments.