| Literature DB >> 22410492 |
Gunnar H Heine1, Alberto Ortiz, Ziad A Massy, Bengt Lindholm, Andrzej Wiecek, Alberto Martínez-Castelao, Adrian Covic, David Goldsmith, Gültekin Süleymanlar, Gérard M London, Gianfranco Parati, Rosa Sicari, Carmine Zoccali, Danilo Fliser.
Abstract
Chronic microinflammation and its cellular hallmark, monocyte activation, contribute substantially to the tremendous burden of cardiovascular disease (CVD) in patients with chronic kidney diseases (CKD). Monocyte heterogeneity is widely acknowledged. Cell-surface expression of CD14 and CD16 defines three functionally and phenotypically distinct subsets of monocytes: classical (CD14(++)CD16(-)) monocytes, intermediate (CD14(++)CD16(+)) monocytes, and nonclassical (CD14(+)CD16(++)) monocytes. A growing body of circumstantial evidence suggests that intermediate monocytes, in particular, contribute to the development of atherosclerosis in the general population as well as in patients with CKD. Intermediate monocytes express a unique pattern of chemokine receptors that have been implicated in atherogenesis. Moreover, this subset of monocytes is predisposed to secrete proinflammatory cytokines. Findings from epidemiological studies indicate that numbers of intermediate monocytes increase with worsening renal function, and that high cell counts predict adverse outcomes in patients undergoing dialysis as well as in patients at early stages of CKD. Based on laboratory and clinical data, intermediate monocytes are a promising therapeutic target for CVD in patients with CKD.Entities:
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Year: 2012 PMID： 22410492 DOI： 10.1038/nrneph.2012.41
Source DB: PubMed Journal: Nat Rev Nephrol ISSN： 1759-5061 Impact factor: 28.314