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001-es BibID:BIBFORM132100
035-os BibID:(scopus)105013847492
Első szerző:Oláh Attila
Cím:Long-term exercise training is associated with unique cardiac troponin I phosphorylation pattern and benign myocardial hypertrophy in the right ventricle in an experimental model of exercise-induced myocardial remodelling / Oláh Attila, Bódi Beáta, Barta Bálint András, Bottlik Olívia, Sayour Alex Ali, Ruppert Mihály, Kolodziejska Karolina Katarzyna, Kovács Andrea, Varga Zoltán V., Ferdinandy Péter, Schilling Oliver, Papp Zoltán, Merkely Béla, Radovits Tamás
Dátum:2025
ISSN:0022-2828
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Molecular And Cellular Cardiology. - 207 (2025), p. 81-91. -
További szerzők:Bódi Beáta (1989-) (molekuláris biológus) Barta Bálint András Bottlik Olívia Sayour, Alex Ali Ruppert Mihály Kolodziejska, Karolina Katarzyna Kovács Andrea Varga Zoltán V. Ferdinándy Péter Schilling, Oliver Papp Zoltán (1965-) (kardiológus, élettanász) Merkely Béla (1965-) (orvos) Radovits Tamás
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM077811
035-os BibID:(WoS)000466833500022 (Scopus)85062460292
Első szerző:Ruppert Mihály
Cím:Myofilament Ca2+ sensitivity correlates with left ventricular contractility during the progression of pressure overload-induced left ventricular myocardial hypertrophy in rats / Mihály Ruppert, Beáta Bódi, Sevil Korkmaz-Icöz, Sivakkanan Loganathan, Weipeng Jiang, Lorenz Lehmann, Attila Oláh, Bálint András Barta, Alex Ali Sayour, Béla Merkely, Matthias Karck, Zoltán Papp, Gábor Szabó, Tamás Radovits
Dátum:2019
ISSN:0022-2828
Megjegyzések:AIM: Here we aimed at investigating the relation between left ventricular (LV) contractility and myofilament function during the development and progression of pressure overload (PO)-induced LV myocardial hypertrophy (LVH). METHODS: Abdominal aortic banding (AB) was performed to induce PO in rats for 6, 12 and 18?weeks. Sham operated animals served as controls. Structural and molecular alterations were investigated by serial echocardiography, histology, quantitative real-time PCR and western blot. LV function was assessed by pressure-volume analysis. Force measurement was carried out in permeabilized cardiomyocytes. RESULTS: AB resulted in the development of pathological LVH as indicated by increased heart weight-to-tibial length ratio, LV mass index, cardiomyocyte diameter and fetal gene expression. These alterations were already present at early stage of LVH (AB-week6). Furthermore, at more advanced stages (AB-week12, AB-week18), myocardial fibrosis and chamber dilatation were also observed. From a hemodynamic point of view, the AB-wk6 group was associated with increased LV contractility, maintained ventriculo-arterial coupling (VAC) and preserved systolic function. In the same experimental group, increased myofilament Ca2+ sensitivity (pCa50) and hyperphosphorylation of cardiac troponin-I (cTnI) at Threonine-144 was detected. In contrast, in the AB-wk12 and AB-wk18 groups, the initial augmentation of LV contractility, as well as the increased myofilament Ca2+ sensitivity and cTnI (Threonine-144) hyperphosphorylation diminished, leading to impaired VAC and reduced systolic performance. Strong correlation was found between LV contractility parameters and myofilament Ca2+-sensitivity among the study groups.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Ca(2+) sensitivity
Contractility
Myocardial hypertrophy
Myofilament function
Megjelenés:Journal of Molecular and Cellular Cardiology. - 129 (2019), p. 208-218. -
További szerzők:Bódi Beáta (1989-) (molekuláris biológus) Korkmaz-Icöz, Sevil Loganathan, Sivakkanan Jiang, Weipeng Lehmann, Lorenz Oláh Attila (sebész) Barta Bálint András Sayour, Alex Ali Merkely Béla (1965-) (orvos) Karck, Matthias Papp Zoltán (1965-) (kardiológus, élettanász) Szabó Gábor (orvos) Radovits Tamás
Pályázati támogatás:ÚNKP-18-3-I-SE-9
ÚNKP
ÚNKP-18-3-III-DE-387
ÚNKP
NVKP-16-1-2016-0017
Egyéb
GINOP-2.3.2-15-2016-00048
GINOP
OTKA11003
OTKA
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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