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J Am Coll Cardiol. 2017 Oct 31;70(18):2278-2289. doi: 10.1016/j.jacc.2017.09.028.

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

Author information

1
Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: plibby@bwh.harvard.edu.

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.

KEYWORDS:

acute coronary syndromes; high-sensitivity C-reactive protein; interleukin-1; myocardial infarction

PMID:
29073957
PMCID:
PMC5687846
DOI:
10.1016/j.jacc.2017.09.028
[Indexed for MEDLINE]
Free PMC Article

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