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Titolo:
Hyper-IL-6 gene therapy reverses fulminant hepatic failure
Autore:
Hecht, N; Pappo, O; Shouval, D; Rose-John, S; Galun, E; Axelrod, JH;
Indirizzi:
Hadassah Med Org, Liver Unit, IL-91120 Jerusalem, Israel Hadassah Med OrgJerusalem Israel IL-91120 t, IL-91120 Jerusalem, Israel Hadassah Med Org, Goldyne Savad Inst Gene Therapy, IL-91120 Jerusalem, Israel Hadassah Med Org Jerusalem Israel IL-91120 y, IL-91120 Jerusalem, Israel Hadassah Med Org, Dept Pathol, IL-91120 Jerusalem, Israel Hadassah Med Org Jerusalem Israel IL-91120 l, IL-91120 Jerusalem, Israel Univ Kiel, Inst Biochem, D-24098 Kiel, Germany Univ Kiel Kiel Germany D-24098 Kiel, Inst Biochem, D-24098 Kiel, Germany
Titolo Testata:
MOLECULAR THERAPY
fascicolo: 5, volume: 3, anno: 2001,
parte:, 1
pagine: 683 - 687
SICI:
1525-0016(200105)3:5<683:HGTRFH>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE LIVER-FAILURE; IN-VIVO; INTERLEUKIN-6; REGENERATION; DEFICIENCY; EFFICIENCY; ADENOVIRUS; INJURY; RATS;
Keywords:
fulminant hepatic failure; gene therapy; hyper-IL-6; IL-6/sIL-6R; gp130 hyperstimulation; D-galactosamine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Axelrod, JH Hadassah Med Org, Liver Unit, POB 12000,Ein Kerem, IL-91120 Jerusalem, Israel Hadassah Med Org POB 12000,Ein Kerem Jerusalem Israel IL-91120
Citazione:
N. Hecht et al., "Hyper-IL-6 gene therapy reverses fulminant hepatic failure", MOL THER, 3(5), 2001, pp. 683-687

Abstract

dFulminant hepatic failure is a catastrophic condition caused by massive hepatocellular apoptosis and necrosis. Inhibition of hepatocyte apoptosis and the enhancement of the endogenous potential for liver regeneration could potentially form an effective basis for treatment of this condition. In response to injury in the liver, IL-6 mediates the acute-phase response and induces both cytoprotective and mitogenic functions. Hyper-IL-6 is a superagonistic designer cytokine consisting of human IL-6 linked by a flexible peptide chain to the secreted form of the IL-6 receptor. In a mouse model of acute liver failure induced by D-galactosamine administration, a single low dose of a hyper-IL-6-encoding adenoviral vector, in contrast to an adeno-IL-6 vector, maintained liver function, prevented the progression of liver necrosis, and induced liver regeneration, leading to dramatically enhanced survival. Thus, hyper-lid gene therapy may be useful for the treatment of fulminant hepatic failure, which is often fatal even following treatment by transplantation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 10:27:16