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

Cardiovascular<b< </b<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 i...
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Gespeichert in:

Autor*in:	Lucie Hénaut [verfasserIn] Alexandre Candellier [verfasserIn] Cédric Boudot [verfasserIn] Maria Grissi [verfasserIn] Romuald Mentaverri [verfasserIn] Gabriel Choukroun [verfasserIn] Michel Brazier [verfasserIn] Saïd Kamel [verfasserIn] Ziad A. Massy [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	cardiovascular calcification chronic kidney disease macrophages monocytes uraemic toxins

Übergeordnetes Werk:	In: Toxins - MDPI AG, 2010, 11(2019), 9, p 529
Übergeordnetes Werk:	volume:11 ; year:2019 ; number:9, p 529

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/toxins11090529

Katalog-ID:	DOAJ025329782

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allfieldsSound	10.3390/toxins11090529 doi (DE-627)DOAJ025329782 (DE-599)DOAJ0ae697d395d5430a8cbb1615c3b2a5cb DE-627 ger DE-627 rakwb eng Lucie Hénaut verfasserin aut New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cardiovascular<b< </b<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. cardiovascular calcification chronic kidney disease macrophages monocytes uraemic toxins Medicine R Alexandre Candellier verfasserin aut Cédric Boudot verfasserin aut Maria Grissi verfasserin aut Romuald Mentaverri verfasserin aut Gabriel Choukroun verfasserin aut Michel Brazier verfasserin aut Saïd Kamel verfasserin aut Ziad A. Massy verfasserin aut In Toxins MDPI AG, 2010 11(2019), 9, p 529 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:11 year:2019 number:9, p 529 https://doi.org/10.3390/toxins11090529 kostenfrei https://doaj.org/article/0ae697d395d5430a8cbb1615c3b2a5cb kostenfrei https://www.mdpi.com/2072-6651/11/9/529 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2019 9, p 529
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author	Lucie Hénaut
spellingShingle	Lucie Hénaut misc cardiovascular calcification misc chronic kidney disease misc macrophages misc monocytes misc uraemic toxins misc Medicine misc R New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease
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topic_title	New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease cardiovascular calcification chronic kidney disease macrophages monocytes uraemic toxins
topic	misc cardiovascular calcification misc chronic kidney disease misc macrophages misc monocytes misc uraemic toxins misc Medicine misc R
topic_unstemmed	misc cardiovascular calcification misc chronic kidney disease misc macrophages misc monocytes misc uraemic toxins misc Medicine misc R
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title	New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease
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title_full	New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease
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author_browse	Lucie Hénaut Alexandre Candellier Cédric Boudot Maria Grissi Romuald Mentaverri Gabriel Choukroun Michel Brazier Saïd Kamel Ziad A. Massy
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title_sort	new insights into the roles of monocytes/macrophages in cardiovascular calcification associated with chronic kidney disease
title_auth	New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease
abstract	Cardiovascular<b< </b<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.
abstractGer	Cardiovascular<b< </b<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.
abstract_unstemmed	Cardiovascular<b< </b<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.
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title_short	New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease
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New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

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