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Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model
Published on: August 25, 2020
Chemokines as therapeutic targets for atherosclerotic plaque destabilization and rupture
Isabelle T M N Daissormont1, Adriaan O Kraaijeveld, Erik A L Biessen
1Department of Pathology, Maastricht University Medical Center, P Debyelaan 25, Maastricht 6229 HX, The Netherlands. isabelle.daissormont@path.unimaas.nl
Abstract:
Chemokines are instrumental in the initiation and progression of atherosclerosis. Recent advances in genomic technologies and the recognition of atherosclerosis as an inflammatory disease have given great impetus to studies addressing the relevance of chemokines for the clinically manifest stages of atherosclerosis and acute cardiovascular syndromes. In this paper, we will review the current status of these studies, highlighting those chemokines that have already been associated with plaque destabilization and rupture. We will recapitulate recent epidemiologic, genomic, histopathological and experimental support for the prominent role of particular chemokines in acute cardiovascular syndromes. Collectively, these data underpin the potential of chemokines as biomarkers and/or therapeutic targets, but also expose the lacunae in our understanding of the precise function of chemokines in the atherosclerosis-related disorders and in the efficacy of chemokine-targeted clinical trials.
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