CBS 2019
CBSMD教育中心
中 文

Other Relevant Articles

Abstract

Recommended Article

10-Year Coronary Heart Disease Risk Prediction Using Coronary Artery Calcium and Traditional Risk Factors: Derivation in the MESA (Multi-Ethnic Study of Atherosclerosis) With Validation in the HNR (Heinz Nixdorf Recall) Study and the DHS (Dallas Heart Study) Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond Healthy Behavior, Risk Factor Control, and Survival in the COURAGE Trial Percutaneous Coronary Intervention Readmissions Where Are the Solutions? Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction Impact of Coronary Lesion Complexity in Percutaneous Coronary Intervention: One-Year Outcomes From the Large, Multicentre e-Ultimaster Registry Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents Clinical Implications of Periprocedural Myocardial Injury in Patients Undergoing Percutaneous Coronary Intervention for Chronic Total Occlusion: Role of Antegrade and Retrograde Crossing Techniques

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.