Education

Ph.D. in Pharmacology, Department of Pharmacology, Complutense University, Madrid, Spain, 2005

Current Position

Miguel Servet Researcher, Instituto de Investigación Hospital Universitario La PAZ, Madrid, Spain

Publications (since 2005)

1. Fernandez-Velasco, M., Ruiz-Hurtado, G., Rueda, A., Neco, P., Mercado-Morales, M., Delgado, C., Napolitano, C., Priori, S. G., Richard, S., Gomez, A. M. and Benitah, J. P. (2011). RyRCa²⁺ leak limits cardiac Ca²⁺ window current overcoming the tonic effect of calmodulinin mice. PLoS One 6(6): e20863.
   
2. Smani, T., Calderon-Sanchez, E., Gomez-Hurtado, N., Fernandez-Velasco, M., Cachofeiro, V., Lahera, V., Ordonez, A. and Delgado, C. (2010). Mechanisms underlying the activation of L-type calcium channels by urocortin in rat ventricular myocytes. Cardiovasc Res 87(3): 459-466.
   
3. Prieto, P., Cuenca, J., Traves, P. G., Fernandez-Velasco, M., Martin-Sanz, P. and Bosca, L. (2010). Lipoxin A4 impairment of apoptotic signaling in macrophages: implication of the PI3K/Akt and the ERK/Nrf-2 defense pathways. Cell Death Differ 17(7): 1179-1188.
   
4. Prieto, P., Cuenca, J., Traves, P. G., Fernandez-Velasco, M., Martin-Sanz, P. and Bosca, L. (2010). Lipoxin A4 impairment of apoptotic signaling in macrophages: implication of the PI3K/Akt and the ERK/Nrf-2 defense pathways. Cell Death Differ 17(7): 1179-1188.
   
5. Fernandez-Velasco, M., Rueda, A., Rizzi, N., Benitah, J. P., Colombi, B., Napolitano, C., Priori, S. G., Richard, S. and Gomez, A. M. (2009). Increased Ca²⁺ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia. Circ Res 104(2): 201-209, 212p following 209.
   
6. Loyer, X., Gomez, A. M., Milliez, P., Fernandez-Velasco, M., Vangheluwe, P., Vinet, L., Charue, D., Vaudin, E., Zhang, W., Sainte-Marie, Y., Robidel, E., Marty, I., Mayer, B., Jaisser, F., Mercadier, J. J., Richard, S., Shah, A. M., Benitah, J. P., Samuel, J. L. and Heymes, C. (2008). Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling. Circulation 117(25): 3187-3198.
   
7. Gellen, B., Fernandez-Velasco, M., Briec, F., Vinet, L., LeQuang, K., Rouet-Benzineb, P., Benitah, J. P., Pezet, M., Palais, G., Pellegrin, N., Zhang, A., Perrier, R., Escoubet, B., Marniquet, X., Richard, S., Jaisser, F., Gomez, A. M., Charpentier, F. and Mercadier, J. J. (2008). Conditional FKBP12.6 overexpression in mouse cardiac myocytes prevents triggered ventricular tachycardia through specific alterations in excitation-contraction coupling. Circulation 117(14): 1778-1786.
   
8. Ruiz-Hurtado, G., Fernandez-Velasco, M., Mourelle, M. and Delgado, C. (2007). LA419, a novel nitric oxide donor, prevents pathological cardiac remodeling in pressure-overloaded rats via endothelial nitric oxide synthase pathway regulation. Hypertension 50(6): 1049-1056.
   
9. Pereira, L., Metrich, M., Fernandez-Velasco, M., Lucas, A., Leroy, J., Perrier, R., Morel, E., Fischmeister, R., Richard, S., Benitah, J. P., Lezoualc'h, F. and Gomez, A. M. (2007). The cAMP binding protein Epac modulates Ca²⁺ sparks by a Ca²⁺/calmodulin kinase signalling pathway in rat cardiac myocytes. J Physiol 583(Pt 2): 685-694.
   
10. Fernandez-Velasco, M., Ruiz-Hurtado, G., Hurtado, O., Moro, M. A. and Delgado, C. (2007). TNF-alpha downregulates transient outward potassium current in rat ventricular myocytes through iNOS overexpression and oxidant species generation. Am J Physiol Heart Circ Physiol 293(1): H238-245.
    
11. Fernandez-Velasco, M., Gomez, A. M. and Richard, S. (2006). Unzipping RyR2 in adult cardiomyocytes: getting closer to mechanisms of inherited ventricular arrhythmias? Cardiovasc Res 70(3): 407-409.
    
12. Fernandez-Velasco, M., Ruiz-Hurtado, G. and Delgado, C. (2006). I K1 and I f in ventricular myocytes isolated from control and hypertrophied rat hearts. Pflugers Arch 452(2): 146-154.
    
13. Zicha, S., Fernandez-Velasco, M., Lonardo, G., L'Heureux, N. and Nattel, S. (2005). Sinus node dysfunction and hyperpolarization-activated (HCN) channel subunit remodeling in a canine heart failure model. Cardiovasc Res 66(3): 472-481.