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Targeting TGFβ signaling to inhibit fibroblast activation as a therapy for fibrosis and cancer: Effect of halofuginone
Year:
2008
Source of publication :
Expert Opinion on Drug Discovery
Authors :
Pines, Mark
;
.
Volume :
3
Co-Authors:
Pines, M., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Facilitators :
From page:
11
To page:
20
(
Total pages:
10
)
Abstract:
The fibroblast to myofibroblast transition in wound healing, fibrosis and cancer has emerged as a viable target for pharmacological intervention. The myofibroblasts acquire specific characteristics because of differences in origin and localization, but also share common properties, such as TGFβ signaling. Halofuginone, an inhibitor of the Smad3 phosphorylation, downstream of the TGFβ signaling, inhibits the activation of fibroblasts and their ability to synthesize the extracellular matrix, regardless of their origin or location. Halofuginone prevented the new and stimulated resolution of pre-existing fibrosis of several organs and inhibited the development and progression of various tumors. Moreover, halofuginone synergizes with chemotherapy and reduces the need for high doses of toxic compounds without impairing the treatment efficacy. In fibrosis, where the myofibroblasts are the major participant, halofuginone can be used as a single therapy, whereas in cancer it should be considered in combination with other therapies that affect the tumor cells via different modalities. © 2008 Informa UK Ltd.
Note:
Related Files :
Cancer
cellular distribution
Drug Safety
Fibrosis
Review
transforming growth factor beta
Show More
Related Content
More details
DOI :
10.1517/17460441.3.1.11
Article number:
Affiliations:
Database:
Scopus
Publication Type:
Review
;
.
Language:
English
Editors' remarks:
ID:
19471
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:29
Scientific Publication
Targeting TGFβ signaling to inhibit fibroblast activation as a therapy for fibrosis and cancer: Effect of halofuginone
3
Pines, M., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Targeting TGFβ signaling to inhibit fibroblast activation as a therapy for fibrosis and cancer: Effect of halofuginone
The fibroblast to myofibroblast transition in wound healing, fibrosis and cancer has emerged as a viable target for pharmacological intervention. The myofibroblasts acquire specific characteristics because of differences in origin and localization, but also share common properties, such as TGFβ signaling. Halofuginone, an inhibitor of the Smad3 phosphorylation, downstream of the TGFβ signaling, inhibits the activation of fibroblasts and their ability to synthesize the extracellular matrix, regardless of their origin or location. Halofuginone prevented the new and stimulated resolution of pre-existing fibrosis of several organs and inhibited the development and progression of various tumors. Moreover, halofuginone synergizes with chemotherapy and reduces the need for high doses of toxic compounds without impairing the treatment efficacy. In fibrosis, where the myofibroblasts are the major participant, halofuginone can be used as a single therapy, whereas in cancer it should be considered in combination with other therapies that affect the tumor cells via different modalities. © 2008 Informa UK Ltd.
Scientific Publication
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