M
Marco Foschi
Researcher at University of Florence
Publications - 40
Citations - 3168
Marco Foschi is an academic researcher from University of Florence. The author has contributed to research in topics: MAPK/ERK pathway & Kinase. The author has an hindex of 23, co-authored 40 publications receiving 3058 citations. Previous affiliations of Marco Foschi include Scripps Research Institute & Medical College of Wisconsin.
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Journal ArticleDOI
Liver stiffness measurement predicts severe portal hypertension in patients with HCV-related cirrhosis.
Francesco Vizzutti,Umberto Arena,Roberto Giulio Romanelli,L. Rega,Marco Foschi,Stefano Colagrande,A. Petrarca,S. Moscarella,Giacomo Belli,Anna Linda Zignego,Fabio Marra,Giacomo Laffi,Massimo Pinzani +12 more
TL;DR: LSM represents a non‐invasive tool for the identification of chronic liver disease patients with clinically significant or severe portal hypertension and could be employed for screening patients to be subjected to standard investigations including upper GI endoscopy and hemodynamic studies.
Journal ArticleDOI
Infection of peripheral mononuclear blood cells by hepatitis C virus
Anna Linda Zignego,Anna Linda Zignego,Donatella Macchia,Monica Monti,Valérie Thiers,Marcello Mazzetti,Marco Foschi,Enrico Maggi,Sergio Romagnani,Paolo Gentilini,Christian Bréchot,Christian Bréchot +11 more
TL;DR: The results indicate that HCV infect blood mononuclear cells, thus suggesting that this cellular tropism may play a role in HCV infection.
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Neutrophil‐derived superoxide anion induces lipid peroxidation and stimulates collagen synthesis in human hepatic stellate cells: Role of nitric oxide
Alessandro Casini,Elisabetta Ceni,R. Salzano,P. Biondi,Maurizio Parola,Andrea Galli,Marco Foschi,Alessandra Caligiuri,Massimo Pinzani,Calogero Surrenti +9 more
TL;DR: Results indicate that neutrophil‐derived ROS may contribute to the development of hepatic fibrosis associated with alcoholic hepatitis and NO produced by neutrophils may exert a “protective” antioxidant effect by operating as a scavenger of superoxide anion.
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Transforming Growth Factor-β Induces Collagenase-3 Expression by Human Gingival Fibroblasts via p38 Mitogen-activated Protein Kinase
Laura Ravanti,Lari Häkkinen,Hannu Larjava,Ulpu Saarialho-Kere,Marco Foschi,Jiahuai Han,Veli-Matti Kähäri +6 more
TL;DR: The results show that TGF-β-elicited induction of MMP-13 expression by gingival fibroblasts is dependent on the activity of p38 MAPK and the presence of functional AP-1 dimers, and suggest a role for M MP-13 in rapid turnover of collagenous matrix during repair of gingivals wounds, which heal with minimal scarring.
Journal ArticleDOI
Activation of p38α MAPK Enhances Collagenase-1 (Matrix Metalloproteinase (MMP)-1) and Stromelysin-1 (MMP-3) Expression by mRNA Stabilization
TL;DR: Two distinct and complementary signaling mechanisms mediating induction of M MP-1 and MMP-3 expression in dermal fibroblasts are identified: AP-1-dependent transcriptional activation via the ERK1/2 pathway and AP- 1-independent enhancement via p38α MAPK by mRNA stabilization.