作者: Wanling Xuan , Yulin Liao , Baihe Chen , Qiaobing Huang , Dingli Xu
DOI: 10.1093/CVR/CVR221
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摘要: Aims Fractalkine (FKN) is a newly identified membrane-bound chemokine; its role in myocardial ischaemia and heart failure largely unknown. We attempted to investigate the of FKN or pressure overload-induced ventricular remodelling failure. Methods results FKN-induced changes failure-related genes cultured rat cardiac cells effect on cardiomyocyte injury during anoxia/reoxygenation (A/R) were examined. The direct influence neutralization potential mechanism was also investigated. In mice with failing hearts, expression correlated lung weight/body weight ratio, left fractional shortening, brain natriuretic peptide expression. cells, exposure increased A cardiomyocytes, matrix metalloproteinase-9 fibroblasts, intercellular adhesion molecule-1 microvascular endothelial cells. promoted damage A/R neutralizing antibody treatment improved induced by infarction overload. Neutralizing receptor inhibited activation mitogen-activated protein kinases (MAPKs) hypoxic cardiomyocytes ischaemic myocardium. Conclusion promotes accelerates progress failure, which associated MAPKs.