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001-es BibID:	BIBFORM105581
035-os BibID:	(cikkazonosító)14651 (WOS)000897324400001 (Scopus)85143732443 (PubMed)36498977
Első szerző:	Nagy Norbert (kísérletes farmakológus)
Cím:	Antiarrhythmic and Inotropic Effects of Selective Na+/Ca2+ Exchanger Inhibition : What Can We Learn from the Pharmacological Studies? / Nagy Norbert, Tóth Noémi, Nánási Péter P.
Dátum:	2022
ISSN:	1422-0067
Megjegyzések:	Life-long stable heart function requires a critical balance of intracellular Ca2+. Several ion channels and pumps cooperate in a complex machinery that controls the influx, release, and efflux of Ca2+. Probably one of the most interesting and most complex players of this crosstalk is the Na+/Ca2+ exchanger, which represents the main Ca2+ efflux mechanism; however, under some circumstances, it can also bring Ca2+ into the cell. Therefore, the inhibition of the Na+/Ca2+ exchanger has emerged as one of the most promising possible pharmacological targets to increase Ca2+ levels, to decrease arrhythmogenic depolarizations, and to reduce excessive Ca2+ influx. In line with this, as a response to increasing demand, several more or less selective Na+/Ca2+ exchanger inhibitor compounds have been developed. In the past 20 years, several results have been published regarding the effect of Na+/Ca2+ exchanger inhibition under various circumstances, e.g., species, inhibitor compounds, and experimental conditions; however, the results are often controversial. Does selective Na+/Ca2+ exchanger inhibition have any future in clinical pharmacological practice? In this review, the experimental results of Na+/Ca2+ exchanger inhibition are summarized focusing on the data obtained by novel highly selective inhibitors.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk heart Na+/Ca2+ exchanger arrhythmia Ca2+-handling inotropy
Megjelenés:	International Journal Of Molecular Sciences. - 23 : 23 (2022), p. 14651. -
További szerzők:	Tóth Noémi Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:	FK-129117 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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