Oral imatinib treatment reduces early fibrogenesis but does not prevent progression in the long term
M Neef, M Ledermann, H Saegesser, V Schneider… - Journal of …, 2006 - Elsevier
BACKGROUND/AIMS: Transactivated hepatic stellate cells (HSCs) represent the key source
of extra cellular matrix (ECM) in fibrotic liver. Imatinib, a potent inhibitor of the PDGF receptor
tyrosine kinase, reduces HSC proliferation and fibrogenesis when treatment is initiated
before fibrosis has developed. We tested the antifibrotic potential of imatinib in ongoing liver
injury and in established fibrosis. METHODS: BDL-rats were gavage fed with 20mg/kg/d
imatinib either early (days 0–21) or late (days 22–35) after BDL. Untreated BDL-rats served …
of extra cellular matrix (ECM) in fibrotic liver. Imatinib, a potent inhibitor of the PDGF receptor
tyrosine kinase, reduces HSC proliferation and fibrogenesis when treatment is initiated
before fibrosis has developed. We tested the antifibrotic potential of imatinib in ongoing liver
injury and in established fibrosis. METHODS: BDL-rats were gavage fed with 20mg/kg/d
imatinib either early (days 0–21) or late (days 22–35) after BDL. Untreated BDL-rats served …
