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001-es BibID:	BIBFORM005628
Első szerző:	Édes István Ferenc (kardiológus)
Cím:	Late-stage alterations in myofibrillar contractile function in a transgenic mouse model of dilated cardiomyopathy (Tgalphaq*44) / Edes, I. F., Toth, A., Csanyi, G., Lomnicka, M., Chlopicki, S., Edes, I., Papp, Z.
Dátum:	2008
ISSN:	1095-8584 (Electronic)
Megjegyzések:	Mechanical and biochemical alterations were investigated in permeabilized cardiomyocytes along with the progression of dilated cardiomyopathy (DCM) in a transgenic mouse line overexpressing the activated Galphaq protein (Tgalphaq44). The isometric force, its Ca(2+) sensitivity (pCa(50)) and the turnover rate of the actin-myosin cycle (k(tr)) were determined at sarcomere lengths (SLs) of 1.9 mum and 2.3 mum before (at 4 and 10 months of age) and after hemodynamic decompensation (at 14 and 18 months of age) in Tgalphaq44 cardiomyocytes and in age-matched control cardiomyocytes. The SL-dependence of pCa(50) was not different in Tgalphaq44 and control hearts. In contrast, a significant increase in pCa(50) was observed in the Tgalphaq44 cardiomyocytes (DeltapCa(50): 0.10-0.15 vs. the controls) after 10 months of age that could be diminished by exposures to the catalytic subunit of protein kinase A (PKA). Accordingly, a decline in endogenous PKA activity and decreased troponin I phosphorylation were detected after 10 months in the Tgalphaq44 hearts. Finally, the maximal Ca(2+)-activated force (F(o)) and k(tr) were lower and the passive force (F(passive)) was higher at 18 months in the Tgalphaq44 cardiomyocytes compared to the control. These mechanical alterations were paralleled by a robust increase in beta-myosin heavy chain expression in the Tgalphaq44 hearts. In conclusion, our data suggested that an initial decrease of PKA signaling and subsequent changes in myofilament protein expression may contribute to the development of dilated cardiomyopathy in Tgalphaq44 hearts.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Cardiomyopathy, Dilated Cattle Cells, Cultured Disease Models, Animal Female GTP-Binding Protein alpha Subunits Male Mice Mice, Transgenic Models, Cardiovascular Myocardial Contraction Myocytes, Cardiac Myofibrils
Megjelenés:	Journal of Molecular and Cellular Cardiology. - 45 : 3 (2008), p. 363-372. -
További szerzők:	Tóth Attila (1971-) (biológus) Csányi Gábor Lomnicka, Magdalena Chlopicki, Stefan Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
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001-es BibID:	BIBFORM002144
Első szerző:	Édes István Ferenc (kardiológus)
Cím:	Rate of tension redevelopment is not modulated by sarcomere length in permeabilized human, murine, and porcine cardiomyocytes / Edes I. F., Czuriga D., Csányi G., Chlopicki S., Recchia F. A., Borbély A., Galajda Z., Edes I., van der Velden J., Stienen G. J., Papp Z.
Dátum:	2007
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. - 293 : 1 (2007), p. R20-R29. -
További szerzők:	Czuriga Dániel (1982-) (kardiológus) Csányi Gábor Chlopicki, Stefan Recchia, Fabio A. Borbély Attila (1978-) (kardiológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Édes István (1952-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Papp Zoltán (1965-) (kardiológus, élettanász)
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001-es BibID:	BIBFORM076736
035-os BibID:	(WoS)000501730100012 (Scopus)85075326564
Első szerző:	Maack, Christoph
Cím:	Treatments targeting inotropy : a position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association of the European Society of Cardiology / Christoph Maack, Thomas Eschenhagen, Nazha Hamdani, Frank R. Heinzel, Alexander R. Lyon, Dietmar J. Manstein, Joseph Metzger, Zoltán Papp, Carlo G. Tocchetti, M. Birhan Yilmaz, Stefan D. Anker, Jean-Luc Balligand, Johann Bauersachs, Dirk Brutsaert, Lucie Carrier, Stefan Chlopicki, John G. Cleland, Rudolf A. de Boer, Alexander Dietl, Rodolphe Fischmeister, Veli-Pekka Harjola, Stephane Heymans, Denise Hilfiker-Kleiner, Johannes Holzmeister, Gilles de Keulenaer, Giuseppe Limongelli, Wolfgang A. Linke, Lars H. Lund, Josep Masip, Marco Metra, Christian Mueller, Burkert Pieske, Piotr Ponikowski, Arsen Ristic, Frank Ruschitzka, Petar M. Seferovic, Hadi Skouri, Wolfram H. Zimmermann, Alexandre Mebazaa
Dátum:	2019
ISSN:	0195-668X
Megjegyzések:	Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.
Tárgyszavak:	idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Heart failure Acute decompensated heart failure Inotropes Cardiogenic shock Excitation-contraction coupling Calcium Sarcomeres Mitochondria Energetics Adrenergic receptors Contractility Levosimendan Omecamtiv mecarbil Nitroxyl
Megjelenés:	European Heart Journal. - 40 : 44 (2019), p. 3626-3640. -
További szerzők:	Eschenhagen, Thomas Hamdani, Nazha Heinzel, Frank R. Lyon, Alexander Manstein, Dietmar J. Metzger József Papp Zoltán (1965-) (kardiológus, élettanász) Tocchetti, Carlo G. Yilmaz, Mehmet Birhan Anker, Stefan D. Balligand, Jean-Luc Bauersachs, Johann Brutsaert, Dirk L. Carrier, Lucie Chlopicki, Stefan Cleland, John G. Boer, Rudolf A. de Dietl, Alexander Fischmeister, Rodolphe Harjola, Veli-Pekka Heymans, Stephane Hilfiker-Kleiner, Denise Holzmeister, Johannes De Keulenaer, Gilles Limongelli, Giuseppe Linke, Wolfgang A. Lund, Lars H. Masip, Josep Metra, Marco Mueller, Christian Pieske, Burkert Ponikowski, Piotr Ristić, Arsen D. Ruschitzka, Frank Seferović, Petar M. Skouri, Hadi Zimmermann, Wolfram H. Mebazaa, Alexandre
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