Cholesterol efflux pathways regulate myelopoiesis: A potential link to altered macrophage function in atherosclerosis

Frontiers in Immunology. 2014;5 DOI 10.3389/fimmu.2014.00490

 

Journal Homepage

Journal Title: Frontiers in Immunology

ISSN: 1664-3224 (Online)

Publisher: Frontiers Media S.A.

LCC Subject Category: Medicine: Internal medicine: Specialties of internal medicine: Immunologic diseases. Allergy

Country of publisher: Switzerland

Language of fulltext: English

Full-text formats available: PDF, HTML, ePUB, XML

 

AUTHORS

Andrew James Murphy (Baker IDI Heart and Diabetes Institute)
Andrew James Murphy (Monash University)
Andrew James Murphy (University of New South Wales)
Dragana eDragoljevic (Baker IDI Heart and Diabetes Institute)
Alan Richard Tall (Columbia University)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 14 weeks

 

Abstract | Full Text

Atherosclerotic cardiovascular disease (CVD) is a chronic inflammatory disease of the blood vessels that can lead to myocardial infarction or stroke. The major cell in the atherosclerotic lesion, the macrophage is thought to be an important contributor to the production of inflammatory mediators that exacerbate this disease. Macrophages are generally derived from circulating monocytes, which are in turn produced by hematopoietic stem and multipotential progenitor cells (HSPCs) in the bone marrow and other medullary organs. Recent studies suggest that disruption in cholesterol homeostasis or prolonged exposure to a hypercholesterolemic environment can influence HSPCs to over-produce monocytes, resulting in monocytosis. These monocytes may carry a pre-programed ability to become M1-like macrophages once they enter the atherosclerotic lesion. Future studies may help to differentiate the role of such pre-programming versus responses to local environmental cues in determining M1, M2 or other macrophage phenotypes in atherosclerotic lesions.