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Titolo:
PATHOGENESIS OF LIVER FIBROSIS
Autore:
ALCOLADO R; ARTHUR MJP; IREDALE JP;
Indirizzi:
UNIV SOUTHAMPTON,SOUTHAMPTON GEN HOSP,LEVEL D,S BLOCK,TREMONA RD SOUTHAMPTON SO1 6YD HANTS ENGLAND UNIV SOUTHAMPTON SOUTHAMPTON HANTS ENGLAND
Titolo Testata:
Clinical science
fascicolo: 2, volume: 92, anno: 1997,
pagine: 103 - 112
SICI:
0143-5221(1997)92:2<103:POLF>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; FAT-STORING CELLS; NORMAL RAT-LIVER; SINUSOIDAL ENDOTHELIAL-CELLS; HEPATIC LIPOCYTES SYNTHESIZE; HUMAN FIBRONECTIN RECEPTOR; BASEMENT-MEMBRANE MATRIX; NECROSIS-FACTOR-ALPHA; COLLAGEN TYPE-I; EXTRACELLULAR-MATRIX;
Keywords:
CELL-MATRIX INTERACTION; HEPATIC STELLATE CELLS; LIVER FIBROSIS; MATRIX; MATRIX REGULATION; TISSUE INHIBITOR OF METALLOPROTEINASE-1; TRANSFORMING GROWTH FACTOR BETA;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
121
Recensione:
Indirizzi per estratti:
Citazione:
R. Alcolado et al., "PATHOGENESIS OF LIVER FIBROSIS", Clinical science, 92(2), 1997, pp. 103-112

Abstract

1. Liver fibrosis is a common sequel to diverse liver injuries. It ischaracterized by an accumulation of interstitial collagens and other matrix components. The hepatic stellate cell is pivotal to the pathogenic process. Fibrotic liver injury results in activation of the hepatic stellate cell which undergoes a phenotypic change to a proliferativemyofibroblast-like cell which synthesizes excess interstitial collagens and other matrix components. 2. The process of initiation of activation and its perpetuation result from complex, often interrelated series of signalling mechanisms which converge on this effector cell. Suchmechanisms include alterations in matrix resulting in changed cell-matrix interactions and stimulation by cytokines released from damaged hepatocytes, infiltrating inflammatory cells, Kupffer cells and matrix. Foremost among the profibrotic cytokines is transforming growth factor beta(1).3. Once the hepatic stellate cell is activated the precedingmatrix changes and recurrent injurious stimuli will perpetuate the activated state. 4. Despite the accumulation of excess collagens, the liver retains a capacity for matrix degradation. This capacity may be overwhelmed and any secreted matrix remodelling enzymes may be inhibitedby the concurrently secreted tissue inhibitors of metalloproteinase-1and alpha(2)-macroglobulin. 5. Our understanding of the molecular pathogenesis of liver fibrosis is increasing. It is anticipated that thisknowledge will provide novel therapeutic avenues to treat this disease process.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 09:40:46