| Autor: |
Williams H; Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia.; Westmead Clinical School, The University of Sydney, Westmead, Sydney, NSW 2145, Australia., Mack CD; Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia.; Westmead Clinical School, The University of Sydney, Westmead, Sydney, NSW 2145, Australia., Li SCH; Chemical Pathology, NSW Health Pathology, Westmead Hospital and Institute of Clinical Pathology and Medical Research, Westmead, Sydney, NSW 2145, Australia.; Blacktown/Mt Druitt Clinical School, Blacktown Hospital, Western Sydney University, Blacktown, NSW 2148, Australia., Fletcher JP; Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia.; Westmead Clinical School, The University of Sydney, Westmead, Sydney, NSW 2145, Australia., Medbury HJ; Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia.; Westmead Clinical School, The University of Sydney, Westmead, Sydney, NSW 2145, Australia. |
| Abstrakt: |
Monocytes play a key role in cardiovascular disease (CVD) as their influx into the vessel wall is necessary for the development of an atherosclerotic plaque. Monocytes are, however, heterogeneous differentiating from classical monocytes through the intermediate subset to the nonclassical subset. While it is recognized that the percentage of intermediate and nonclassical monocytes are higher in individuals with CVD, accompanying changes in inflammatory markers suggest a functional impact on disease development that goes beyond the increased proportion of these 'inflammatory' monocyte subsets. Furthermore, emerging evidence indicates that changes in monocyte proportion and function arise in dyslipidemia, with lipid lowering medication having some effect on reversing these changes. This review explores the nature and number of monocyte subsets in CVD addressing what they are, when they arise, the effect of lipid lowering treatment, and the possible implications for plaque development. Understanding these associations will deepen our understanding of the clinical significance of monocytes in CVD. |
