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001-es BibID:	BIBFORM030336
035-os BibID:	PMID: 15320833
Első szerző:	Mohácsi Attila (orvos)
Cím:	Effects of endothelins on cardiac and vascular cells : new therapeutic target for the future? / Attila Mohácsi, János Magyar, Tamás Bányász, Péter P. Nánási
Dátum:	2004
ISSN:	1570-1611 (Linking)
Megjegyzések:	The predominant isoform of the endothelin peptide family. endothelin-1 (ET-1)exerts various biological effects. These include effects on arterial smoothmuscle cells causing intense vasoconstriction and stimulation of cardiac cells.ET-1 promotes changes in cardiomyocytes that are consistent with electricalremodelling such as changes in ionic current density and inhomogeneousprolongation of action potential duration resulting in increased dispersion. Asfor the underlying mechanisms, ET-1 was shown to suppress several cAMP-dependentionic currents, such as ICa, IK and ICl in various mammalian cardiac preparationsincluding human myocytes; however, the degree of suppression of these currents isdifferent and highly dependent on experimental conditions. The proposedarrhythmogenic effects of ET-1 may also involve enhancement of Ca2+ release fromintracellular stores, generation of IP3, and acidosis due to stimulation of theNa+/H+ exchange. Furthermore, ET-1 acts as the natural counterpart toendothelium-derived nitric oxide, which exerts vasodilator, antithrombotic andantiproliferative effects, and inhibits leukocyte adhesion to the vascular wall.Effects of ET-1 are mediated through interaction with two major types of cellsurface receptors. ETA receptors have been associated with electricalremodelling, vasoconstriction and cell growth, while ETB receptors are involvedin the clearance of ET-1, inhibition of endothelial apoptosis, release of NO andprostacyclins, and inhibition of the expression of ET-1 converting enzyme. Thederangement of endothelial function in various cardiovascular diseases, such ascardiomyopathies, hypertension or arteriosclerosis, is a crucial element of thepathomechanism, thus ET receptors are considered as important therapeutictargets. Indeed, ET receptor antagonists may be able to preserve or restoreendothelial integrity and may have antiarrhythmic properties; therefore, they arepromising tools in cardiovascular medicine.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban 0 (Endothelin-1) 0 (Endothelins) 0 (Protein Isoforms) 0 (Receptors, Endothelin) 7440-70-2 (Calcium) Animals Calcium/*metabolism Electric Stimulation Endothelin-1/adverse effects/metabolism/physiology Endothelins/antagonists & inhibitors/biosynthesis/physiology Humans Muscle, Smooth, Vascular/drug effects/metabolism/physiology Myocardial Contraction/drug effects/physiology Myocytes, Cardiac/drug effects/metabolism Protein Isoforms Receptors, Endothelin/antagonists & inhibitors Signal Transduction/drug effects Vasoconstriction/drug effects/physiology Ventricular Fibrillation/drug therapy egyetemen (Magyarországon) készült közlemény
Megjelenés:	Current vascular pharmacology. - 2 : 1 (2004), p. 53-63. -
További szerzők:	Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM081578
035-os BibID:	(PMID)30963976
Első szerző:	Muscogiuri, Giovanna
Cím:	Calcium and Vitamin D Supplementation : myths and Realities with Regard to Cardiovascular Risk / Giovanna Muscogiuri, Luigi Barrea, Barbara Altieri, Carolina Di Somma, Harjit Pal Bhattoa, Daniela Laudisio, Guillaume T. Duval, Gabriella Pugliese, Cédric Annweiler, Francesco Orio, Hana Fakhouri, Silvia Savastano, Annamaria Colao
Dátum:	2019
ISSN:	1570-1611
Megjegyzések:	Vitamin D and calcium are considered crucial for the treatment of bone diseases. Both vitamin D and calcium contribute to bone homeostasis but also preserve muscle health by reducing the risk of falls and fractures. Low vitamin D concentrations result in secondary hyperparathyroidism and contribute to bone loss, although the development of secondary hyperparathyroidism varies, even in patients with severe vitamin D deficiency. Findings from observational studies have shown controversial results regarding the association between bone mineral density and vitamin D/calcium status, thus sparking a debate regarding optimum concentrations of 25-hydroxyvitamin D and calcium for the best possible skeletal health. Although most of the intervention studies reported a positive effect of supplementation with calcium and vitamin D on bone in patients with osteoporosis, this therapeutic approach has been a matter of debate regarding potential side effects on the cardiovascular (CV) system. Thus, the aim of this review is to consider the current evidence on the physiological role of vitamin D and calcium on bone and muscle health. Moreover, we provide an overview on observational and interventional studies that investigate the effect of vitamin D and calcium supplementation on bone health, also taking into account the possible CV side-effects. We also provide molecular insights on the effect of calcium plus vitamin D on the CV system.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Vitamin D bone health calcium cardiovascular system myocardial infarction stroke
Megjelenés:	Current Vascular Pharmacology. - 17 : 6 (2019), p. 610-617. -
További szerzők:	Barrea, Luigi Altieri, Barbara Di Somma, Carolina Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Laudisio, Daniela Duval, Guillaume Pugliese, Gabriella Annweiler, Cedric Orio, Francesco Fakhoury, Hana M. A. Savastano, Silvia Colao, Annamaria
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM003605
Első szerző:	Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:	Structure and function of poly(ADP-ribose) polymerase-1 : role in oxidative stress-related pathologies / Virág L.
Dátum:	2005
Megjegyzések:	Poly(ADP-ribosyl) ation is a reversible post-translational protein modification implicated in the regulation of a number of biological functions. Whereas an 18 member superfamily of poly(ADP-ribose) polymerase (PARP) enzymes synthesize poly(ADP-ribose) (PAR), a single protein, PAR glycohydrolase (PARG) is responsible for the catabolism of the polymer. PARP-1 accounts for more than 90% of the poly(ADP-ribosyl)ating capacity of the cells. PARP-1 activated by DNA breaks cleaves NAD(+) into nicotinamide and ADP-ribose and uses the latter to synthesize long branching PAR polymers covalently attached to acceptor proteins including histones, DNA repair enzymes, transcription factors and PARP-1. Whereas activation of PARP-1 by mild genotoxic stimuli may facilitate DNA repair and cell survival, irreparable DNA damage triggers apoptotic or necrotic cell death. In apoptosis, early PARP activation may assist the apoptotic cascade [e.g. by stabilizing p53, by mediating the translocation of apoptosis inducing factor (AIF) from the mitochondria to the nucleus or by inhibiting early activation of DNases]. In most severe oxidative stress situations, excessive DNA damage causes over activation of PARP-1, which incapacitates the apoptotic machinery and switches the mode of cell death from apoptosis to necrosis. Besides serving as a cytotoxic mediator, PARP-1 is also involved in transcriptional regulation, most notably in the NF kappaB and AP-1 driven expression of inflammatory mediators. Pharmacological inhibition or genetic ablation of PARP-1 provided remarkable protection from tissue injury in various oxidative stress-related disease models ranging from stroke, diabetes, diabetic endothelial dysfunction, myocardial ischemia-reperfusion, shock, Parkinson's disease, arthritis, colitis to dermatitis and uveitis. These beneficial effects are attributed to inhibition of the PARP-1 mediated suicidal pathway and to reduced expression of inflammatory cytokines and other mediators (e.g. inducible nitric oxide synthase).
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban poly(ADP-ribose) polymerase cytotoxicity necrosis apoptosis DNA damage peroxynitrite
Megjelenés:	Current Vascular Pharmacology. - 3 : 3 (2005), p. 209-214. -
Internet cím:	elektronikus változat
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