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- W2056476377 abstract "Background: Midkine (MK), a heparin-binding growth factor, has various functions such as migration of inflammatory cell and anti-apoptotic effect. We reported serum MK levels were increased in patients with heart failure and were independently associated with adverse cardiac events. The aim of this study was to examine the role of MK in cardiac hypertrophy and remodeling. Methods and Results: We generated transgenic mice overexpressing MK (MK-Tg) in a heart-specific manner. Transverse aortic constriction (TAC) or sham operation were performed in MK-Tg and wild-type (WT) mice. After 4 weeks of TAC, the ratio of left ventricular weight to body weight was significantly increased in MK-Tg mice than in WT mice. MK-Tg mice showed significant dilatation of left ventricular end-diastolic dimension and reduction of cardiac function compared with WT mice. Expression of cardiac fetal genes and profibrotic genes were significantly higher in MK-Tg mice than in WT mice. Consistent with these results, MK-Tg mice developed more cardiomyocyte hypertrophy and interstitial fibrosis. In the hearts of MK-Tg mice, phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 after TAC occurred earlier compared with WT mice. Conclusion: MK exacerbates cardiac hypertrophy and remodeling via early ERK 1/2 phosphorylation in pressure overload model." @default.
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- W2056476377 date "2011-09-01" @default.
- W2056476377 modified "2023-09-23" @default.
- W2056476377 title "Midkine Exacerbates Pressure Overload-induced Cardiac Hypertrophy and Remodeling in Transgenic Mice" @default.
- W2056476377 doi "https://doi.org/10.1016/j.cardfail.2011.06.588" @default.
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