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Association of CYP2C19 Loss-of-Function Alleles with Major Adverse Cardiovascular Events of Clopidogrel in Stable Coronary Artery Disease Patients Undergoing Percutaneous Coronary Intervention: Meta-analysis Incidence, Predictors, and Outcomes of In-Hospital Percutaneous Coronary Intervention Following Coronary Artery Bypass Grafting Five-Year Outcomes after PCI or CABG for Left Main Coronary Disease Drug-Coated Balloon Versus Drug-Eluting Stent in Primary Percutaneous Coronary Intervention: A Feasibility Study Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease Home-Based Cardiac Rehabilitation: A Scientific Statement From the American Association of Cardiovascular and Pulmonary Rehabilitation, the American Heart Association, and the American College of Cardiology Double kissing crush in left main coronary bifurcation lesions: A crushing blow to the rival stenting techniques Long-term outcomes of rotational atherectomy of underexpanded stents. A single center experience Contrast-Associated Acute Kidney Injury and Serious Adverse Outcomes Following Angiography 2020 AHA/ACC Key Data Elements and Definitions for Coronary Revascularization A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (Writing Committee to Develop Clinical Data Standards for Coronary Revascularization)

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.