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001-es BibID:	BIBFORM023025
Első szerző:	Gozzelino, Raffaella
Cím:	Mechanisms of Cell Protection by Heme Oxygenase-1 / Gozzelino Raffaella, Jeney Viktoria, Soares Miguel P.
Dátum:	2010
ISSN:	0362-1642
Megjegyzések:	Heme oxygenases (140) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe(2+), carbon monoxide (CO), and biliverdin. The stress-responsive HO-1 isoenzyme affords protection against programmed cell death. The mechanism underlying this cytoprotective effect relies on the ability of HO-1 to catabolize free heme and prevent it from sensitizing cells to undergo programmed cell death. This cytoprotective effect inhibits the pathogenesis of a variety of immune-mediated inflammatory diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Annual Review Of Pharmacology And Toxicology. - 50 : 1 (2010), p. 323-354. -
További szerzők:	Jeney Viktória (1971-) (vegyész, kémia tanár) Soares, Miguel P.
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001-es BibID:	BIBFORM023024
Első szerző:	Larsen, Rasmus
Cím:	A Central Role for Free Heme in the Pathogenesis of Severe Sepsis / Larsen, R., Gozzelino, R., Jeney, V., Tokaji, L., Bozza, F. A., Japiassu, A. M., Bonaparte, D., Cavalcante, M. M., Chora, A., Ferreira, A., Marguti, I., Cardoso, S., Sepulveda, N., Smith, A., Soares, M. P.
Dátum:	2010
ISSN:	1946-6234
Megjegyzések:	Low-grade polymicrobial infection induced by cecal ligation and puncture is lethal in heme oxygenase-1-deficient mice (Hmox1(-/-)), but not in wild-type (Hmox1(+/+)) mice. Here we demonstrate that the protective effect of this heme-catabolizing enzyme relies on its ability to prevent tissue damage caused by the circulating free heme released from hemoglobin during infection. Heme administration after low-grade infection in mice promoted tissue damage and severe sepsis. Free heme contributed to the pathogenesis of severe sepsis irrespective of pathogen load, revealing that it compromised host tolerance to infection. Development of lethal forms of severe sepsis after high-grade infection was associated with reduced serum concentrations of the heme sequestering protein hemopexin (HPX), whereas HPX administration after high-grade infection prevented tissue damage and lethality. Finally, the lethal outcome of septic shock in patients was also associated with reduced HPX serum concentrations. We propose that targeting free heme by HPX might be used therapeutically to treat severe sepsis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Science Translational Medicine. - 2 : 51 (2010), p. 1-12. -
További szerzők:	Gozzelino, Raffaella Jeney Viktória (1971-) (vegyész, kémia tanár) Tokaji László Bozza, Fernando A. Japiassú, André M. Bonaparte, Dolores Cavalcante, Moisés Marinho Chora, Angelo Ferreira, Ana Marguti, Ivo Cardoso, Sílvia Sepúlveda, Nuno Smith, Ann Soares, Miguel P.
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001-es BibID:	BIBFORM078365
035-os BibID:	(WoS)000461679000073 (Scopus)85063288166 (PMID)30833408
Első szerző:	Ramos, Susana
Cím:	Renal control of disease tolerance to malaria / Susana Ramos, Ana Rita Carlos, Balamurugan Sundaram, Viktoria Jeney, Ana Ribeiro, Raffaella Gozzelino, Claudia Bank, Erida Gjini, Faouzi Braza, Rui Martins, Temitope Wilson Ademolue, Birte Blankenhaus, Zélia Gouveia, Pedro Faísca, Damian Trujillo, Sílvia Cardoso, Sofia Rebelo, Laura del Barrio, Abolfazl Zarjou, Subhashini Bolisetty, Anupam Agarwal, Miguel P. Soares
Dátum:	2019
ISSN:	0027-8424 1091-6490
Megjegyzések:	Malaria, the disease caused by Plasmodium spp. infection, remains a major global cause of morbidity and mortality. Host protection from malaria relies on immune-driven resistance mechanisms that kill Plasmodium However, these mechanisms are not sufficient per se to avoid the development of severe forms of disease. This is accomplished instead via the establishment of disease tolerance to malaria, a defense strategy that does not target Plasmodium directly. Here we demonstrate that the establishment of disease tolerance to malaria relies on a tissue damage-control mechanism that operates specifically in renal proximal tubule epithelial cells (RPTEC). This protective response relies on the induction of heme oxygenase-1 (HMOX1; HO-1) and ferritin H chain (FTH) via a mechanism that involves the transcription-factor nuclear-factor E2-related factor-2 (NRF2). As it accumulates in plasma and urine during the blood stage of Plasmodium infection, labile heme is detoxified in RPTEC by HO-1 and FTH, preventing the development of acute kidney injury, a clinical hallmark of severe malaria.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk disease tolerance heme infection kidney malaria
Megjelenés:	Proceedings of the National Academy of Sciences of the United States of America. - 116 : 12 (2019), p. 5681-5686. -
További szerzők:	Carlos, Ana Rita Sundaram, Balamurugan Jeney Viktória (1971-) (vegyész, kémia tanár) Ribeiro, Ana Gozzelino, Raffaella Bank, Claudia Gjini, Erida Braza, Faouzi Martins, Rui Ademolue, Temitope Wilson Blankenhaus, Birte Gouveia, Zélia Faísca, Pedro Trujillo, Damian Cardoso, Sílvia Rebelo, Sofia del Barrio, Laura Zarjou, Abolfazl (1979-) (kutató orvos) Bolisetty, Subhashini Agarwal, Anupam Soares, Miguel P.
Pályázati támogatás:	OTKA-116024 OTKA
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