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J. Hamzavi

Researcher at Heidelberg University

Publications -  7
Citations -  952

J. Hamzavi is an academic researcher from Heidelberg University. The author has contributed to research in topics: Hepatic stellate cell & Transforming growth factor. The author has an hindex of 6, co-authored 7 publications receiving 889 citations. Previous affiliations of J. Hamzavi include RWTH Aachen University.

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Smad7 prevents activation of hepatic stellate cells and liver fibrosis in rats.

TL;DR: Gen transfer of Smad7 inhibits experimental fibrogenesis in vivo and suggests that the underlying mechanisms involve inhibition of TGF-beta signaling and HSC transdifferentiation.
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Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage

TL;DR: The data indicate that hepatocytes undergo TGF-beta-dependent EMT-like phenotypic changes and actively participate in fibrogenesis and ablation of T GF-beta signaling specifically in this cell type is sufficient to blunt the fibrogenic response.
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Id1 is a critical mediator in TGF-β–induced transdifferentiation of rat hepatic stellate cells†

TL;DR: In conclusion, Id1 is identified as TGF‐β/ALK1/Smad1 target gene in HSCs and represents a critical mediator of transdifferentiation that might be involved in hepatic fibrogenesis.
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Profibrogenic transforming growth factor‐β/activin receptor–like kinase 5 signaling via connective tissue growth factor expression in hepatocytes

TL;DR: Evidence is provided for the profibrogenic activity of TGF‐β directed to hepatocytes and mediated via the up‐regulation of CTGF, which can be hindered by an activated activin receptor–like kinase 1 pathway and completely inhibited by T GF‐β antagonist Smad7.
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Disruption of the Smad7 gene enhances CCI4‐dependent liver damage and fibrogenesis in mice

TL;DR: It is concluded that Smad7 mediates a protective effect from adverse TGF‐β signalling in damaged liver, re‐iterating its negative regulatory loop on signalling.