Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Vincenzo Prestigiacomo"'
Publikováno v:
PLoS ONE, Vol 13, Iss 7, p e0201044 (2018)
Hepatic stellate cells (HSC) orchestrate the deposition of extracellular matrix (ECM) and are the primary effector of liver fibrosis. Several factors, including TGF-β1, PDGF and oxidative stress, have been shown to trigger HSC activation. However, t
Externí odkaz:
https://doaj.org/article/17218222633b49239a553c33ed2527fd
Publikováno v:
PLoS ONE, Vol 12, Iss 6, p e0179995 (2017)
Currently most liver fibrosis research is performed in vivo, since suitable alternative in vitro systems which are able to recapitulate the cellular events leading to liver fibrosis are lacking. Here we aimed at generating a system containing cells r
Externí odkaz:
https://doaj.org/article/e749945b756e441dbf456b3056909393
Autor:
Martin Pirkl, Fabiana Lüönd, Gerhard Christofori, Niko Beerenwinkel, Mizue Hisano, Ravi Kr Kalathur, Vincenzo Prestigiacomo
Publikováno v:
Life Science Alliance, 5 (2)
Life Science Alliance
Life Science Alliance
In melanoma, a switch from a proliferative melanocytic to an invasive mesenchymal phenotype is based on dramatic transcriptional reprogramming which involves complex interactions between a variety of signaling pathways and their downstream transcript
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d37ef7c89f9f25dfe5dd62f50a425da6
https://hdl.handle.net/20.500.11850/521394
https://hdl.handle.net/20.500.11850/521394
Publikováno v:
Journal of pharmacological and toxicological methods. 101
Chronic liver damage can lead to fibrosis, encompassing hepatocellular injury, activation of Kupffer cells (KC), and activation of hepatic stellate cells (HSC). Inflammation and TGF-β1 are known mediators in the liver fibrosis adverse outcome pathwa
Publikováno v:
PLoS ONE
PLoS ONE, Vol 12, Iss 6, p e0179995 (2017)
PLoS ONE, Vol 12, Iss 6, p e0179995 (2017)
Background & aims Currently most liver fibrosis research is performed in vivo, since suitable alternative in vitro systems which are able to recapitulate the cellular events leading to liver fibrosis are lacking. Here we aimed at generating a system
Publikováno v:
Toxicology Letters. 280:S277