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001-es BibID:	BIBFORM010415
Első szerző:	Borbély Attila (kardiológus)
Cím:	Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium / Borbely, A., Falcao-Pires, I., van Heerebeek, L., Hamdani, N., Edes, I., Gavina, C., Leite-Moreira, A. F., Bronzwaer, J. G. F., Papp, Z., van der Velden, J., Stienen, G. J. M., Paulus, W. J.
Dátum:	2009
ISSN:	1524-4571 (Electronic)
Megjegyzések:	High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of isolated cardiomyocytes to expression of titin isoforms and to phosphorylation of titin and titin isoforms. Biopsies were procured by transvascular technique (44 HF, 3 CON), perioperatively (25 AS, 4 CON), or from explanted hearts (4 HF, 8 CON). None had coronary artery disease. Isolated, permeabilized cardiomyocytes were stretched to 2.2-microm sarcomere length to measure F(passive). Expression and phosphorylation of titin isoforms were analyzed using gel electrophoresis with ProQ Diamond and SYPRO Ruby stains and reported as ratio of titin (N2BA/N2B) or of phosphorylated titin (P-N2BA/P-N2B) isoforms. F(passive) was higher in HF (6.1+/-0.4 kN/m(2)) than in CON (2.3+/-0.3 kN/m(2); P<0.01) or in AS (2.2+/-0.2 kN/m(2); P<0.001). Titin isoform expression differed between HF (N2BA/N2B=0.73+/-0.06) and CON (N2BA/N2B=0.39+/-0.05; P<0.001) and was comparable in HF and AS (N2BA/N2B=0.59+/-0.06). Overall titin phosphorylation was also comparable in HF and AS, but relative phosphorylation of the stiff N2B titin isoform was significantly lower in HF (P-N2BA/P-N2B=0.77+/-0.05) than in AS (P-N2BA/P-N2B=0.54+/-0.05; P<0.01). Relative hypophosphorylation of the stiff N2B titin isoform is a novel mechanism responsible for raised F(passive) of human HF cardiomyocytes.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Aged Biopsy Elasticity Female Heart Failure Humans Male Middle Aged Muscle Proteins Myocardium Myocytes, Cardiac Phosphorylation Protein Isoforms Protein Kinases Sarcomeres
Megjelenés:	Circulation Research. - 104 : 6 (2009), p. 780-786. -
További szerzők:	Falcao-Pires, Ines Heerebeek, Loek, van Hamdani, Nazha Édes István (1952-) (kardiológus) Gavina, Cristina Leite-Moreira, Adelino F. Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Velden, Jolanda, van der Stienen, Ger J. M. Paulus, Walter J.
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001-es BibID:	BIBFORM088825
035-os BibID:	(WoS)000581770400028
Első szerző:	Kovács Á.
Cím:	Omecamtiv mecarbil evokes electromechanical alternans in control rat hearts / Kovács Á., Fülöp G. Á., Csípő T., Nagy L., Bódi B., Fagyas M., Lind-Helgadottir S., Pórszász R., Horváth B., Nánási P., Oláh A., Radovits T., Merkely B., Hamdani N., Édes I., Csanádi Z., Tóth A., Papp Z.
Dátum:	2018
ISSN:	0022-2828
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idézhető absztrakt folyóiratcikk
Megjelenés:	Journal Of Molecular And Cellular Cardiology. - 120 (2018), p. 11. -
További szerzők:	Fülöp Gábor Áron (1988-) (általános orvos) Csípő Tamás (1990-) Nagy L. Bódi Beáta (absztraktok) Fagyas Miklós (1984-) (orvos) Lind-Helgadottir, S. Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Horváth Balázs (1981-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Oláh Attila (sebész) Radovits Tamás Merkely Béla (1965-) (orvos) Hamdani, Nazha Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Tóth Adrienn (1988-) (molekuláris biológus, élettanász) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP
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001-es BibID:	BIBFORM088270
035-os BibID:	(cikkazonosító)470 (WoS)000600100200006 (scopus)85097316669
Első szerző:	Lódi Mária
Cím:	Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy / Mária Lódi, Viktor Bánhegyi, Beáta Bódi, Alexandra Gyöngyösi, Árpád Kovács, Anita Árokszállási, Nazha Hamdani, Miklós Fagyas, István Édes, Zoltán Csanádi, István Czuriga, Zoltán Kisvárday, István Lekli, Péter Bai, Attila Tóth, Zoltán Papp, Dániel Czuriga
Dátum:	2020
ISSN:	1479-5876
Megjegyzések:	BackgroundCardiomyopathy is a common side effect of doxorubicin (DOX) chemotherapy. Despite intensive research efforts in the field, there is still no evidence available for routine cardioprotective prophylaxis to prevent cardiotoxicity in the majority of oncological patients at low risk of cardiovascular disease. We have recently demonstrated the advantages of a prophylactic, combined heart failure therapy in an experimental model of DOX-induced cardiomyopathy. In the current work, we focus on individually applied prophylactic medications studied in the same translational environment to clarify their distinct roles in the prevention of DOX cardiotoxicity.MethodsTwelve-week-old male Wistar rats were divided into 5 subgroups. Prophylactic beta -blocker (BB, bisoprolol), angiotensin-converting enzyme inhibitor (ACEI, perindopril) or aldosterone antagonist (AA, eplerenone) treatments were applied 1 week before DOX administration, then 6 cycles of intravenous DOX chemotherapy were administered. Rats receiving only intravenous DOX or saline served as positive and negative controls. Blood pressure, heart rate, body weight, and echocardiographic parameters were monitored in vivo. Two months after the last DOX administration, the animals were sacrificed, and their heart and serum samples were frozen in liquid nitrogen for histological, mechanical, and biochemical measurements.ResultsAll prophylactic treatments increased the survival of DOX-receiving animals. The lowest mortality rates were seen in the BB and ACEI groups. The left ventricular ejection fraction was only preserved in the BB group. The DOX-induced increase in the isovolumetric relaxation time could not be prevented by any prophylactic treatment. A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments.ConclusionPrimary prophylaxis with cardioprotective agents like BB or ACEI has a key role in the prevention of DOX-induced cardiotoxicity in healthy rats. Future human studies are necessary to implement this finding in the clinical management of oncological patients free of cardiovascular risk factors.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk doxorubicin anthracycline cardiotoxicity animal model heart failure
Megjelenés:	Journal of Translational Medicine. - 18 : 1 (2020), p. 470. -
További szerzők:	Bánhegyi Viktor (1991-) (kardiológus) Bódi Beáta (1989-) (molekuláris biológus) Gyöngyösi Alexandra (1990-) (táplálkozástudományi szakember) Kovács Árpád (1986-) (kardiológus) Árokszállási Anita (1982-) (orvos) Hamdani, Nazha Fagyas Miklós (1984-) (orvos) Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Czuriga István (1948-2018) (kardiológus) Kisvárday Zoltán (1957-) (biológus, neurobiológus) Lekli István (1981-) (gyógyszerész) Bai Péter (1976-) (biokémikus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Czuriga Dániel (1982-) (kardiológus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP EFOP-3.6.2-16-2017-00006 EFOP
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