CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

What's new in the Fourth Universal Definition of Myocardial infarction? Prognostic Significance of Complex Ventricular Arrhythmias Complicating ST-Segment Elevation Myocardial Infarction Left Main Revascularization in 2017 Coronary Artery Bypass Grafting or Percutaneous Coronary Intervention? Patterns and associations between DAPT cessation and 2-year clinical outcomes in left main/proximal LAD versus other PCI: Results from the Patterns of Non-Adherence to Dual Antiplatelet Therapy in Stented Patients (PARIS) registry Relation between door-to-balloon times and mortality after primary percutaneous coronary intervention over time: a retrospective study Comparison of double kissing crush versus Culotte stenting for unprotected distal left main bifurcation lesions: results from a multicenter, randomized, prospective DKCRUSH-III study Respiratory syncytial virus infection and risk of acute myocardial infarction Improvement of Clinical Outcome in Patients With ST-Elevation Myocardial Infarction Between 1999 And 2016 in China : The Prospective, Multicenter Registry MOODY Study In Vivo Calcium Detection by Comparing Optical Coherence Tomography, Intravascular Ultrasound, and Angiography Recurrent Cardiovascular Events in Survivors of Myocardial Infarction with St-Segment Elevation (From the AMI-QUEBEC 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.