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J Cell Mol Med. 2018 Mar;22(3):1366-1382. doi: 10.1111/jcmm.13462. Epub 2018 Jan 24.

The role of monocytosis and neutrophilia in atherosclerosis.

Author information

1
Department of Neurochemistry, Division of Basic and Applied Neurobiology, Serbsky Federal Medical Research Center of Psychiatry and Narcology, Moscow, Russia.
2
Federal Scientific Clinical Center for Resuscitation and Rehabilitation, Moscow, Russia.
3
Skolkovo Innovative Center, Institute for Atherosclerosis Research, Moscow, Russia.
4
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Sciences, Moscow, Russia.

Abstract

Monocytosis and neutrophilia are frequent events in atherosclerosis. These phenomena arise from the increased proliferation of hematopoietic stem and multipotential progenitor cells (HSPCs) and HSPC mobilization from the bone marrow to other immune organs and circulation. High cholesterol and inflammatory signals promote HSPC proliferation and preferential differentiation to the myeloid precursors (i.e., myelopoiesis) that than give rise to pro-inflammatory immune cells. These cells accumulate in the plaques thereby enhancing vascular inflammation and contributing to further lesion progression. Studies in animal models of atherosclerosis showed that manipulation with HSPC proliferation and differentiation through the activation of LXR-dependent mechanisms and restoration of cholesterol efflux may have a significant therapeutic potential.

KEYWORDS:

atherosclerosis; atherosclerotic plaque; chemokines; inflammation; monocyte; neutrophil

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