Cited 39 times since 2004 (2 per year) source: EuropePMC Journal of the American College of Cardiology, Volume 44, Issue 5, 1 1 2004, Pages 1113-1123 Fibroblast growth factor-1 improves cardiac functional recovery and enhances cell survival after ischemia and reperfusion: a fibroblast growth factor receptor, protein kinase C, and tyrosine kinase-dependent mechanism. Palmen M, Daemen MJ, De Windt LJ, Willems J, Dassen WR, Heeneman S, Zimmermann R, Van Bilsen M, Doevendans PA
Objectives
We sought to investigate the role of fibroblast growth factor (FGF)-1 during acute myocardial ischemia and reperfusion.
Background
The FGFs display cardioprotective effects during ischemia and reperfusion.
Methods
We investigated FGF-1-induced cardioprotection during ischemia and reperfusion and the intracellular signaling pathways responsible for these effects in an ex vivo murine setup of myocardial ischemia and reperfusion.
Results
Cardiac-specific human FGF-1 overexpression was associated with enhanced post-ischemic hemodynamic recovery and decreased lactate dehydrogenase release during reperfusion. Inhibition of the FGF receptor, protein kinase C (PKC), and tyrosine kinase (TK) resulted in blockade of FGF-1-induced protective effects on cardiac functional recovery and cell death.
Conclusions
The overexpression of FGF-1 induces cardioprotection through a pathway that involves the FGF receptor, PKC, and TK.
