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Titolo:
Apoptosis in sepsis: a new target for therapeutic exploration
Autore:
Oberholzer, C; Oberholzer, A; Clare-Salzler, M; Moldawer, LL;
Indirizzi:
Univ Florida, Coll Med, Dept Surg, Gainesville, FL 32610 USA Univ FloridaGainesville FL USA 32610 ept Surg, Gainesville, FL 32610 USA Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 Lab Med, Gainesville, FL 32610 USA
Titolo Testata:
FASEB JOURNAL
fascicolo: 6, volume: 15, anno: 2001,
pagine: 879 - 892
SICI:
0892-6638(200104)15:6<879:AISANT>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; PROGRAMMED CELL-DEATH; INFLAMMATORY RESPONSE SYNDROME; BCL-2 FAMILY PROTEINS; ACTIVATION-INDUCED APOPTOSIS; DELAYS NEUTROPHIL APOPTOSIS; FULMINANT LIVER DESTRUCTION; SOLUBLE FAS LIGAND; CYTOCHROME-C;
Keywords:
Bcl-2; caspases; lymphocytes; neutrophils;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
126
Recensione:
Indirizzi per estratti:
Indirizzo: Moldawer, LL Univ Florida, Shands Hosp, Coll Med, Dept Surg, Room 6116,1600 SW Archer Rd,POB 100286, Gainesville, FL 32610 USA Univ Florida Room 6116,1600 SW Archer Rd,POB 100286 Gainesville FL USA 32610
Citazione:
C. Oberholzer et al., "Apoptosis in sepsis: a new target for therapeutic exploration", FASEB J, 15(6), 2001, pp. 879-892

Abstract

The treatment of sepsis and septic shock remains a clinical conundrum, andrecent prospective trials with biological response modifiers aimed at the inflammatory response have shown only modest clinical benefit. Recently, interest has shifted toward therapies aimed at reversing the accompanying periods of immune suppression. Studies in experimental animals and critically ill patients have demonstrated that increased apoptosis of lymphoid organs and some parenchymal tissues contributes to this immune suppression, anergy, and organ system dysfunction, During sepsis syndromes, lymphocyte apoptosis can be triggered by the absence of IL-2 or by the release of glucocorticoids, granzymes, or the so-called 'death' cytokines: tumor necrosis factor alpha or Fas ligand, Apoptosis proceeds via auto-activation of cytosolic and/or mitochondrial caspases, which can be influenced by the pro- and anti-apoptotic members of the Bcl-2 family, In experimental animals, not only cantreatment with inhibitors of apoptosis prevent lymphoid cell apoptosis; itmay also improve outcome. Although clinical trials with anti-apoptotic agents remain distant due in large part to technical difficulties associated with their administration and tissue targeting, inhibition of lymphocyte apoptosis represents an attractive therapeutic target for the septic patient.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 00:00:02