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Heart Failure With Preserved Ejection Fraction in the Young Intravascular ultrasound-guided implantation of drug-eluting stents to improve outcome: a meta-analysis Treatment strategies for coronary in-stent restenosis: systematic review and hierarchical Bayesian network meta-analysis of 24 randomised trials and 4880 patients In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis Economic and Quality-of-Life Outcomes of Natriuretic Peptide–Guided Therapy for Heart Failure Left Main Revascularization With PCI or CABG in Patients With Chronic Kidney Disease: EXCEL Trial Non-obstructive High-Risk Plaques Increase the Risk of Future Culprit Lesions Comparable to Obstructive Plaques Without High-Risk Features: The ICONIC Study Use of Intravascular Ultrasound Imaging in Percutaneous Coronary Intervention to Treat Left Main Coronary Artery Disease Patient Selection and Clinical Outcomes in the STOPDAPT-2 Trial: An All-Comer Single-Center Registry During the Enrollment Period of the STOPDAPT-2 Randomized Controlled Trial Mechanical complications of everolimus-eluting stents associated with adverse events: an intravascular ultrasound study

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.