期刊
TOXINS
卷 11, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/toxins11090529
关键词
cardiovascular calcification; chronic kidney disease; macrophages; monocytes; uraemic toxins
资金
- La Federation Hospitalo-Universitaire 'Early Markers of Cardiovascular Remodeling in Valvulopathy and Heart Failure' (FHU REMOD VHF)
- French National Research Agency as part of the French government's Investissements d'Avenir program [ANR-16-RHUS-0003_STOP-AS]
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据