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Un-JAMming atherosclerotic arteries: JAM-L as a target to attenuate plaque development.

Authors
  • Sokeechand, B Sumayyah H1
  • Trigatti, Bernardo L2
  • 1 Department of Biochemistry and Biomedical Sciences and Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada. , (Canada)
  • 2 Department of Biochemistry and Biomedical Sciences and Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada [email protected] , (Canada)
Type
Published Article
Journal
Clinical Science
Publisher
Portland Press
Publication Date
Jul 31, 2019
Volume
133
Issue
14
Pages
1581–1585
Identifiers
DOI: 10.1042/CS20190541
PMID: 31331991
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Atherosclerosis is a chronic inflammatory disease and a major driver of heart attack and stroke. Atherosclerosis development is driven by the infiltration of leukocytes, including monocytes and neutrophils, among other inflammatory cells into the artery wall, monocyte differentiation to macrophages and uptake of oxidized low density lipoprotein. Macrophage activation and inflammatory cytokine production are major factors which drive ongoing inflammation and plaque development. Identification of novel pathways driving this on-going inflammatory process may provide new opportunities for therapeutic intervention. In their article published in Clinical Science (2019) (vol 133, 1215-1228), Sun and colleagues demonstrate a novel role for the junction adhesion molecule-like (JAML) protein in driving on-going atherosclerotic plaque inflammation and plaque development. They report that JAML is expressed in macrophages and other cells in atherosclerotic plaques in both humans and mice, and that silencing JAML expression attenuates atherosclerotic plaque progression in mouse models of early and late stage plaque development. They demonstrate that JAML is required for oxidized-low density lipoprotein (OxLDL)-induced up-regulation of inflammatory cytokine production by macrophages, pointing to it as a potential therapeutic target for reducing ongoing plaque inflammation. © 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

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