Találati lista | Tudóstér

001-es BibID:	BIBFORM108774
035-os BibID:	(cikkazonosító)102629 (WoS)000944336500001 (Scopus)85147884917
Első szerző:	Combi Zsolt
Cím:	Hydrogen sulfide as an anti-calcification stratagem in human aortic valve : altered biogenesis and mitochondrial metabolism of H2S lead to H2S deficiency in calcific aortic valve disease / Zsolt Combi, László Potor, Péter Nagy, Katalin Éva Sikura, Tamás Ditrói, Eszter Petra Jurányi, Klaudia Galambos, Tamás Szerafin, Péter Gergely, Matthew Whiteman, Roberta Torregrossa, Yuchao Ding, Lívia Beke, Zoltán Hendrik, Gábor Méhes, György Balla, József Balla
Dátum:	2023
ISSN:	2213-2317
Megjegyzések:	Hydrogen sulfide (H2S) was previously revealed to inhibit osteoblastic differentiation of valvular interstitial cells (VICs), a pathological feature in calcific aortic valve disease (CAVD). This study aimed to explore the metabolic control of H2S levels in human aortic valves. Lower levels of bioavailable H2S and higher levels of interleukin-1? (IL-1?) and tumor necrosis factor-? (TNF-?) were detected in aortic valves of CAVD patients compared to healthy individuals, accompanied by higher expression of cystathionine ?-lyase (CSE) and same expression of cystathionine ?-synthase (CBS). Increased biogenesis of H2S by CSE was found in the aortic valves of CAVD patients which is supported by increased production of lanthionine. In accordance, healthy human aortic VICs mimic human pathology under calcifying conditions, as elevated CSE expression is associated with low levels of H2S. The expression of mitochondrial enzymes involved in H2S catabolism including sulfide quinone oxidoreductase (SQR), the key enzyme in mitochondrial H2S oxidation, persulfide dioxygenase (ETHE1), sulfite oxidase (SO) and thiosulfate sulfurtransferase (TST) were up-regulated in calcific aortic valve tissues, and a similar expression pattern was observed in response to high phosphate levels in VICs. AP39, a mitochondria-targeting H2S donor, rescued VICs from an osteoblastic phenotype switch and reduced the expression of IL-1? and TNF-? in VICs. Both pro-inflammatory cytokines aggravated calcification and osteoblastic differentiation of VICs derived from the calcific aortic valves. In contrast, IL-1? and TNF-? provided an early and transient inhibition of VICs calcification and osteoblastic differentiation in healthy cells and that effect was lost as H2S levels decreased. The benefit was mediated via CSE induction and H2S generation. We conclude that decreased levels of bioavailable H2S in human calcific aortic valves result from an increased H2S metabolism that facilitates the development of CAVD. CSE/H2S represent a pathway that reverses the action of calcifying stimu
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Arteriosclerosis Chronic kidney disease Hydrogen sulfide Mitochondrial H(2)S catabolism Phosphate Valvular inflammation Vascular calcification Érelmeszesedés Krónikus vesebetegség Hidrogén-szulfid Mitokondriális H(2)S katabolizmus Foszfát Valvuláris gyulladás Vaszkuláris meszesedés
Megjelenés:	Redox Biology. - 60 (2023), p. 1-19. -
További szerzők:	Potor László Nagy Péter (1976-) (vegyész) Sikura Katalin Éva (1985-) (biológus) Ditrói Tamás (1989-) (vegyész) Jurányi Eszter Petra Galambos Klaudia (1995-) (biológus) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Gergely Péter (1974-) (igazságügyi orvosszakértő) Whiteman, Matthew Torregrossa, Roberta Ding, Yuchao (1995-) (Ph.D. hallgató) Beke Lívia Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 (IRONHEARTH) GINOP EFOP-3.6.2-16-2017-00006 (LIVE LONGER) EFOP TKP2020-NKA-04 Egyéb TKP2021-EGA-18 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: