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New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

1
EA 7517 MP3CV, CURS, F-80054 Amiens, France
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Faculty of Medicine, University of Picardie Jules Verne, F-80000 Amiens, France
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Division of Nephrology, Amiens-Picardie University Hospital, F-80054 Amiens, France
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Department of Biochemistry, Amiens-Picardie University Hospital, F-80054 Amiens, France
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Faculty of Pharmacy, University of Picardie Jules Verne, F-80000 Amiens, France
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Division of Nephrology, Ambroise Paré University Hospital, APHP, F-92104 Boulogne-Billancourt, France
7
Inserm U1018 –Team 5, CESP, UVSQ, University Paris-Saclay, F-94807 Villejuif, France
*
Authors to whom correspondence should be addressed.
Toxins 2019, 11(9), 529; https://doi.org/10.3390/toxins11090529
Received: 18 July 2019 / Revised: 6 September 2019 / Accepted: 9 September 2019 / Published: 12 September 2019
(This article belongs to the Special Issue The Chronic Kidney Disease - Mineral Bone Disorder (CKD-MBD))
Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.
Keywords: cardiovascular calcification; chronic kidney disease; macrophages; monocytes; uraemic toxins cardiovascular calcification; chronic kidney disease; macrophages; monocytes; uraemic toxins
MDPI and ACS Style

Hénaut, L.; Candellier, A.; Boudot, C.; Grissi, M.; Mentaverri, R.; Choukroun, G.; Brazier, M.; Kamel, S.; Massy, Z.A. New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease. Toxins 2019, 11, 529.

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