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001-es BibID:	BIBFORM030699
Első szerző:	Czuriga Dániel (kardiológus)
Cím:	Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure / Czuriga Dániel, Tóth Attila, Pásztor Enikő T., Balogh Ágnes, Bodnár Andrea, Nizsalóczki Enikő, Lionetti Vincenzo, Recchia Fabio A., Czuriga István, Édes István, Papp Zoltán
Dátum:	2012
ISSN:	0300-8428
Megjegyzések:	We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca2+ sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation waswider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42; P = 0.0047) or that of the free wall of the control animals (IQR = 0.36; P = 0.0093). Additionally, the Ca2+ sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca2+ sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Egészség- és Környezettudomány Cardiac function Pacing-induced heart failure Beta-adrenergic signaling Dilated cardiomyopathy Cardiac troponin I
Megjelenés:	Basic Research In Cardiology. - 107 : 2 (2012), p. 1-13. -
További szerzők:	Tóth Attila (1971-) (biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Balogh Ágnes (1984-) (kardiológus) Dóczy-Bodnár Andrea (1970-) (biofizikus) Nizsalóczki Enikő Lionetti, Vincenzo Recchia, Fabio A. Czuriga István (1948-2018) (kardiológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Vascularis rizikó- és stroke betegek vizsgálata TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Membrán dinamika
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001-es BibID:	BIBFORM030675
Első szerző:	Czuriga Dániel (kardiológus)
Cím:	Cardiac aging : a review / Czuriga, D., Papp, Z., Czuriga, I., Balogh, Á.
Dátum:	2011
ISSN:	1682-8631
Megjegyzések:	Background: Physiology of aging includes numerous modifications at different levels of the cardiovascular system, resulting in adverse remodeling of the heart and blood vessels. Methods: The present review aims to summarize the different mechanisms in detail during the process of aging with special emphasis on the neurohumoral regulation, autophagy, and remodeling of the extracellular matrix (ECM). Results: Age-associated cellular and molecular mechanisms involve cardiomyocyte function, alterations of neurohormonal regulation, as well as changes in the ECM. Moreover, interactions between the distinct territories involved in the age-related modifications increase the complexity of senescence-associated cardiovascular remodeling. Altered adrenergic and renin-angiotensin systems control neurohormonal regulation of age-associated cardiovascular function. Increased oxidative stress induces enhanced production of cellular waste material, and facilitates the detrimental effects of aging on senescent cardiomyocytes, which are unable to maintain their homeostasis and redox equilibrium due to altered autophagic capacity. Increased collagen and advanced glycation endproducts (AGEs) deposition in the ECM further worsen global function of the aging heart. Conclusions: During the aging process, several modifications in the heart and blood vessels occur at different levels of the cardiovascular system. This adverse remodeling is further influenced by a number of cross-talk actions between the separate mechanisms. Further investigations are needed to elucidate the exact cause-effect relations among the underlying mechanisms, and to clarify their hierarchical position during the course of the aging process.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Egészség- és Környezettudomány Senescence Neurohumoral regulation Cardiomyocytes Autophagy Fibrosis
Megjelenés:	European Surgery (Acta Chirurgica Austriaca). - 43 : 2 (2011), p. 69-77. -
További szerzők:	Papp Zoltán (1965-) (kardiológus, élettanász) Czuriga István (1948-2018) (kardiológus) Balogh Ágnes (1984-) (kardiológus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Vascularis rizikó- és stroke betegek vizsgálata K 68363 OTKA
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