ArticleArteriosclerosis, thrombosis, and vascular biology2015
Cluster of differentiation 43 deficiency in leukocytes leads to reduced atherosclerosis--brief report.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Chitosan from Crabs (Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Article
- Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2021Article
- Chronic skin inflammation accelerates macrophage cholesterol crystal formation and atherosclerosis.JCI insight · 2018Article
- Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveThe aim of this study was to investigate the role of cluster of differentiation 43 (CD43), an integral membrane glycoprotein with both proadhesive and antiadhesive activities, in atherosclerosis. APPROACH AND
resultsLow-density lipoprotein receptor-deficient mice were lethally irradiated and reconstituted with either bone marrow from CD43(-/-) mice or from wild-type controls. We found that mice lacking the CD43 on their leukocytes had significantly less severe atherosclerosis and that, contrary to our expectation, macrophage infiltration into the vessel wall was not affected by the lack of CD43 in the leukocytes. However, we found that CD43 mediates cholesterol homeostasis in macrophages by facilitating cholesterol efflux. This resulted in a significant reduction in storage of cholesterol in the aorta of mice lacking CD43 in the leukocytes.
conclusionsCD43 may be an important mediator of macrophage lipid homeostasis, thereby affecting macrophage foam cell formation and ultimately atherosclerotic plaque development.
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Registered trials
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