Zobrazeno 1 - 4
of 4
pro vyhledávání: '"I G Lunde"'
Autor:
K Rypdal, A O Melleby, E L Robinson, S Palmero, D Seifert, D Martin, K Andreassen, C P Dahl, I Sjaastad, T Toennessen, M Stokke, S Heymans, G Christensen, S Apte, I G Lunde
Publikováno v:
European Heart Journal. 43
Background/Introduction Cardiac fibrosis is a central pathophysiological process accompanying most cardiac diseases including heart failure, and is a predictor of poor outcomes. The fibrotic process is mediated by activated cardiac fibroblasts (CFBs)
Autor:
S L V M Stroeks, J A J Verdonschot, I G Lunde, M T H M Henkens, M Willemars, F Schianchi, J F P Luiken, P Wang, K Derks, I P C Krapels, E K Vanhoutte, E A V Jones, H G Brunner, M Nabben, S R B Heymans
Publikováno v:
European Heart Journal. 43
Background/Objectives Titin truncating variants (TTNtv) are the most prevalent genetic cause of dilated cardiomyopathy (DCM), resulting in upregulation of cardiac transcripts of oxidative phosphorylation (1,2). However, the underlying molecular mecha
Autor:
A. Leone, I. Aquila, C. Vicinanza, C. Iaconetti, A. Bochicchio, S. Ottolenghi, C. Indolfi, B. Nadal-Ginard, G. M. Ellison, D. Torella, C. Mias, G. Genet, C. Guilbeau-Frugier, A. Pathak, J. M. Senard, C. Gales, A. D. Egorova, P. S. J. Khedoe, M. T. H. Goumans, S. M. Nauli, P. Ten Dijke, R. E. Poelmann, B. P. Hierck, M. Miragoli, M. J. Lab, A. Singh, M. Sikkel, A. Lyon, J. Gorelik, C. Cheung, A. S. Bernardo, M. W. Trotter, R. A. Pedersen, S. Sinha, M. Mioulane, G. Foldes, S. E. Harding, B. Reglin, T. W. Secomb, A. R. Pries, M. Buckingham, F. Lescroart, S. Meilhac, J.-F. Le Garrec, N. Rozmaritsa, T. Christ, E. Wettwer, M. Knaut, U. Ravens, S. Tokar, S. Schobesberger, P. T. Wright, A. R. Lyon, A. Van Mil, S. Grundmann, M.-J. Goumans, S. Jaksani, P. A. Doevendans, J. P. Sluijter, A. J. Tijsen, A. S. Amin, J. R. Giudicessi, M. W. Tanck, C. R. Bezzina, E. E. Creemers, A. M. Wilde, M. J. Ackerman, Y. M. Pinto, C. Gedicke-Hornung, V. Behrens-Gawlik, D. Khajetoorians, G. Mearini, S. Reischmann, B. Geertz, T. Voit, P. Dreyfus, T. Eschenhagen, L. Carrier, G. D. Duerr, J. C. Heinemann, D. Wenzel, A. Ghanem, J. C. Alferink, A. Zimmer, B. Lutz, A. Welz, B. K. Fleischmann, O. Dewald, M. Sbroggio', A. Bertero, L. Giuliano, M. Brancaccio, G. Tarone, M. Meiser, M. Kohlhaas, Y. Chen, G. Csordas, G. Dorn, C. Maack, B. Stapel, M. Hoch, A. Haghikia, P. Fischer, D. Hilfiker-Kleiner, B. Schroen, M. Corsten, W. Verhesen, L. De Windt, S. Zacchigna, T. Thum, P. Carmeliet, A. Papageorgiou, S. Heymans, I. G. Lunde, A. V. Finsen, G. Florholmen, B. Skrbic, H. Kvaloy, H. O. Jarstadmarken, I. Sjaastad, T. Tonnessen, C. R. Carlson, G. Christensen, J. Paavola, S. Schliffke, S. Rossetti, I. Kuo, S. Yuan, Z. Sun, P. Harris, V. Torres, B. Ehrlich, P. Robinson, K. Adams, Y.-H. Zhang, B. Casadei, H. Watkins, C. Redwood, A. N. Seneviratne, J. E. Cole, M. E. Goddard, Z. Mohri, A. J. Cross, R. Krams, C. Monaco, B. R. Everaert, S. J. Van Laere, V. Y. Hoymans, J. P. Timmermans, C. J. Vrints
Publikováno v:
Cardiovascular Research. 93:S46-S51
Publikováno v:
The Journal of cardiovascular surgery. 56(3)
Visfatin may play a part in reverse left ventricular remodelling. Using a mouse model of reversible left ventricle pressure overload, we examined if visfatin was altered in the myocardium. Furthermore, we addressed this issue in patients with aortic