4.7 Review

Inflammation, Immunity, and Infection in Atherothrombosis JACC Review Topic of the Week

Journal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 72, Issue 17, Pages 2071-2081

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2018.08.1043

Keywords

basic & translational research

Funding

  1. National Heart, Lung, and Blood Institute (NHLBI) [HL080472, U01HL28606, R01HL076801]
  2. RRM Charitable Fund
  3. National Institutes of Health (NIH) [HL119145, HG007690, GM107618, HL061795]
  4. American Heart Association grant Scaling the Computation of Predicting Drug Protein Interactions
  5. National Institute of Allergy and Infectious Diseases [K24AI112393]
  6. NIH [R01HL125034, R01DE014079]
  7. Novartis
  8. Kowa
  9. Pfizer
  10. Amgen

Ask authors/readers for more resources

Observations on human and experimental atherosclerosis, biomarker studies, and now a large-scale clinical trial support the operation of immune and inflammatory pathways in this disease. The factors that incite innate and adaptive immune responses implicated in atherogenesis and in lesion complication include traditional risk factors such as protein and lipid components of native and modified low-density lipoprotein, angiotensin II, smoking, visceral adipose tissue, and dys-metabolism. Infectious processes and products of the endogenous microbiome might also modulate atherosclerosis and its complications either directly, or indirectly by eliciting local and systemic responses that potentiate disease expression. Trials with antibiotics have not reduced recurrent cardiovascular events, nor have vaccination strategies yet achieved clinical translation. However, anti-inflammatory interventions such as anticytokine therapy and colchicine have begun to show efficacy in this regard. Thus, inflammatory and immune mechanisms can link traditional and emerging risk factors to atherosclerosis, and offer novel avenues for therapeutic intervention. (c) 2018 the American College of Cardiology Foundation. Published by Elsevier. All rights reserved.

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