Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/121424
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Type: Journal article
Title: Inflammation as a therapeutic target in atherosclerosis
Author: Nguyen, M.T.
Fernando, S.
Schwarz, N.
Tan, J.T.
Bursill, C.A.
Psaltis, P.J.
Citation: Journal of Clinical Medicine, 2019; 8(8):1109-1-1109-20
Publisher: MDPI
Issue Date: 2019
ISSN: 2077-0383
2077-0383
Statement of
Responsibility: 
Mau T Nguyen, Sanuja Fernando, Nisha Schwarz, Joanne TM Tan, Christina A Bursill and Peter J Psaltis
Abstract: Atherosclerotic coronary artery disease (CAD) results from build-up of cholesterol-rich plaques in the walls of the coronary arteries and is a leading cause of death. Inflammation is central to atherosclerosis. Uncontrolled inflammation makes coronary plaques "unstable" and vulnerable to rupture or erosion, leading to thrombosis and myocardial infarction (MI). As multiple inflamed plaques often co-exist in the coronary system, patients are at risk of repeated atherothrombotic cardiovascular events after MI, with rates of 10-12% at one year and 18-20% at three years. This is largely because current therapies for CAD, such as lipid-lowering statins, do not adequately control plaque inflammation. New anti-atherosclerotic agents are therefore needed, especially those that better target inflammation. The recent positive results for the anti-interleukin-1-beta (IL-1β) monoclonal antibody, Canakinumab, in the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) clinical trial has provided a major stimulant to the field. It highlights that not only is inflammation important from a pathogenic and risk prediction perspective in CAD, but that reducing inflammation can be beneficial. The challenge is now to find the best strategies to achieve this in real-world practice. This review outlines the role that inflammation plays in atherosclerosis and provides an update on anti-inflammatory therapies currently being investigated to target atherosclerosis.
Keywords: Inflammation; atherosclerosis; C-reactive protein; canakinumab; methotrexate; colchicine; interleukin
Rights: © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
RMID: 0030127609
DOI: 10.3390/jcm8081109
Grant ID: http://purl.org/au-research/grants/nhmrc/1127159
http://purl.org/au-research/grants/nhmrc/1161506
Appears in Collections:Medicine publications

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