CBS 2019
CBSMD教育中心
中 文

科学研究

Abstract

Recommended Article

1-Year Outcomes After Edge-to-Edge Valve Repair for Symptomatic Tricuspid Regurgitation: Results From the TriValve Registry Comparison of plaque characteristics in narrowings with ST-elevation myocardial infarction (STEMI), non-STEMI/unstable angina pectoris and stable coronary artery disease (from the ADAPT-DES IVUS Substudy) Use of IVUS guided coronary stenting with drug eluting stent: a systematic review and meta-analysis of randomized controlled clinical trials and high quality observational studies Provisional versus elective two-stent strategy for unprotected true left main bifurcation lesions: Insights from a FAILS-2 sub-study Reduced Apolipoprotein M and Adverse Outcomes Across the Spectrum of Human Heart Failure Updated Expert Consensus Statement on Platelet Function and Genetic Testing for Guiding P2Y12 Receptor Inhibitor Treatment in Percutaneous Coronary Intervention rhACE2 Therapy Modifies Bleomycin-Induced Pulmonary Hypertension via Rescue of Vascular Remodeling Management of Antithrombotic Therapy in Atrial Fibrillation Patients Undergoing PCI: JACC State-of-the-Art Review

Review Article2017 Oct 31;70(18):2278-2289.

JOURNAL:J Am Coll Cardiol. Article Link

Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond

Libby P Keywords: acute coronary syndromes; high-sensitivity C-reactive protein; interleukin-1; myocardial infarction

ABSTRACT


Inflammatory pathways drive atherogenesis and link conventional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1β) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients.