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1-Year Outcomes of Patients Undergoing Primary Angioplasty for Myocardial Infarction Treated With Prasugrel Versus Ticagrelor Risk of Myocardial Infarction in Anticoagulated Patients With Atrial Fibrillation Association Between Diastolic Dysfunction and Health Status Outcomes in Patients Undergoing Transcatheter Aortic Valve Replacement Off-hour presentation and outcomes in patients with acute myocardial infarction: systematic review and meta-analysis Canadian SCAD Cohort Study: Shedding Light on SCAD From a United Front Prognostic Value of Fractional Flow Reserve Measured Immediately After Drug-Eluting Stent Implantation Impact of age and comorbidity on risk stratification in idiopathic pulmonary arterial hypertension Long-Term Coronary Functional Assessment of the Infarct-Related Artery Treated With Everolimus-Eluting Bioresorbable Scaffolds or Everolimus-Eluting Metallic Stents: Insights of the TROFI II Trial A sirolimus-eluting bioabsorbable polymer-coated stent (MiStent) versus an everolimus-eluting durable polymer stent (Xience) after percutaneous coronary intervention (DESSOLVE III): a randomised, single-blind, multicentre, non-inferiority, phase 3 trial A Novel Circulating MicroRNA for the Detection of Acute Myocarditis

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.