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Article: Hepatic Myofibroblasts: A Heterogeneous and Redox-Modulated Cell Population in Liver Fibrogenesis.

Bocca, Claudia / Protopapa, Francesca / Foglia, Beatrice / Maggiora, Marina / Cannito, Stefania / Parola, Maurizio / Novo, Erica

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 7

Abstract: During chronic liver disease (CLD) progression, hepatic myofibroblasts (MFs) represent a unique cellular phenotype that plays a critical role in driving liver fibrogenesis and then fibrosis. Although they could originate from different cell types, MFs ... ...

Abstract	During chronic liver disease (CLD) progression, hepatic myofibroblasts (MFs) represent a unique cellular phenotype that plays a critical role in driving liver fibrogenesis and then fibrosis. Although they could originate from different cell types, MFs exhibit a rather common pattern of pro-fibrogenic phenotypic responses, which are mostly elicited or sustained both by oxidative stress and reactive oxygen species (ROS) and several mediators (including growth factors, cytokines, chemokines, and others) that often operate through the up-regulation of the intracellular generation of ROS. In the present review, we will offer an overview of the role of MFs in the fibrogenic progression of CLD from different etiologies by focusing our attention on the direct or indirect role of ROS and, more generally, oxidative stress in regulating MF-related phenotypic responses. Moreover, this review has the purpose of illustrating the real complexity of the ROS modulation during CLD progression. The reader will have to keep in mind that a number of issues are able to affect the behavior of the cells involved: a) the different concentrations of reactive species, b) the intrinsic state of the target cells, as well as c) the presence of different growth factors, cytokines, and other mediators in the extracellular microenvironment or of other cellular sources of ROS.
Language	English
Publishing date	2022-06-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11071278
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Hypoxia, Hypoxia-Inducible Factors and Liver Fibrosis.

Foglia, Beatrice / Novo, Erica / Protopapa, Francesca / Maggiora, Marina / Bocca, Claudia / Cannito, Stefania / Parola, Maurizio

Cells

2021 Volume 10, Issue 7

Abstract: Liver fibrosis is a potentially reversible pathophysiological event, leading to excess deposition of extracellular matrix (ECM) components and taking place as the net result of liver fibrogenesis, a dynamic and highly integrated process occurring during ... ...

Abstract	Liver fibrosis is a potentially reversible pathophysiological event, leading to excess deposition of extracellular matrix (ECM) components and taking place as the net result of liver fibrogenesis, a dynamic and highly integrated process occurring during chronic liver injury of any etiology. Liver fibrogenesis and fibrosis, together with chronic inflammatory response, are primarily involved in the progression of chronic liver diseases (CLD). As is well known, a major role in fibrogenesis and fibrosis is played by activated myofibroblasts (MFs), as well as by macrophages and other hepatic cell populations involved in CLD progression. In the present review, we will focus the attention on the emerging pathogenic role of hypoxia, hypoxia-inducible factors (HIFs) and related mediators in the fibrogenic progression of CLD.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Humans ; Hypoxia/complications ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/complications ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/pathology ; Neovascularization, Pathologic ; Signal Transduction
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors
Language	English
Publishing date	2021-07-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10071764
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: In vivo

Novo, Erica / Cannito, Stefania / Parola, Maurizio

Stem cell investigation

2016 Volume 3, Page(s) 53

Language	English
Publishing date	2016-09-29
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2884645-X
ISSN	2313-0792 ; 2306-9759
ISSN (online)	2313-0792
ISSN	2306-9759
DOI	10.21037/sci.2016.09.08
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Histidine-rich glycoprotein in metabolic dysfunction-associated steatohepatitis-related disease progression and liver carcinogenesis.

Foglia, Beatrice / Sutti, Salvatore / Cannito, Stefania / Rosso, Chiara / Maggiora, Marina / Casalino, Alice / Bocca, Claudia / Novo, Erica / Protopapa, Francesca / Ramavath, Naresh Naik / Provera, Alessia / Gambella, Alessandro / Bugianesi, Elisabetta / Tacke, Frank / Albano, Emanuele / Parola, Maurizio

Frontiers in immunology

2024 Volume 15, Page(s) 1342404

Abstract: Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously non-alcoholic fatty liver disease (NAFLD), is a leading cause of chronic liver disease worldwide. In 20%-30% of MASLD patients, the disease progresses to metabolic ... ...

Abstract	Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously non-alcoholic fatty liver disease (NAFLD), is a leading cause of chronic liver disease worldwide. In 20%-30% of MASLD patients, the disease progresses to metabolic dysfunction-associated steatohepatitis (MASH, previously NASH) which can lead to fibrosis/cirrhosis, liver failure as well as hepatocellular carcinoma (HCC). Here we investigated the role of histidine-rich glycoprotein (HRG), a plasma protein produced by hepatocytes, in MASLD/MASH progression and HCC development. Methods: The role of HRG was investigated by morphological, cellular, and molecular biology approaches in (a) HRG Results: In non-neoplastic settings, murine and clinical data indicate that HRG increases significantly in parallel with disease progression. In particular, in MASLD/MASH patients, higher levels of HRG plasma levels were detected in subjects with extensive fibrosis/cirrhosis. When submitted to the pro-carcinogenic protocol, HRG Conclusion: Murine and clinical data indicate that HRG plays a significant role in MASLD/MASH progression to HCC by supporting a specific population of tumor-associated macrophages with pro-inflammatory response and pro-angiogenetic capabilities which critically support cancer cell survival. Furthermore, our data suggest HRG as a possible prognostic predictor in HCC patients with MASLD/MASH-related HCCs.
MeSH term(s)	Humans ; Animals ; Mice ; Carcinoma, Hepatocellular/etiology ; Liver Neoplasms/etiology ; Metabolic Diseases ; Carcinogenesis ; Non-alcoholic Fatty Liver Disease ; Liver Cirrhosis/etiology ; Disease Progression ; Acetamides ; Proteins
Chemical Substances	histidine-rich proteins ; CDAA (93-71-0) ; Acetamides ; Proteins
Language	English
Publishing date	2024-02-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1342404
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Hepatic Myofibroblasts: A Heterogeneous and Redox-Modulated Cell Population in Liver Fibrogenesis

Bocca, Claudia / Protopapa, Francesca / Foglia, Beatrice / Maggiora, Marina / Cannito, Stefania / Parola, Maurizio / Novo, Erica

Antioxidants. 2022 June 28, v. 11, no. 7

2022

Abstract	During chronic liver disease (CLD) progression, hepatic myofibroblasts (MFs) represent a unique cellular phenotype that plays a critical role in driving liver fibrogenesis and then fibrosis. Although they could originate from different cell types, MFs exhibit a rather common pattern of pro-fibrogenic phenotypic responses, which are mostly elicited or sustained both by oxidative stress and reactive oxygen species (ROS) and several mediators (including growth factors, cytokines, chemokines, and others) that often operate through the up-regulation of the intracellular generation of ROS. In the present review, we will offer an overview of the role of MFs in the fibrogenic progression of CLD from different etiologies by focusing our attention on the direct or indirect role of ROS and, more generally, oxidative stress in regulating MF-related phenotypic responses. Moreover, this review has the purpose of illustrating the real complexity of the ROS modulation during CLD progression. The reader will have to keep in mind that a number of issues are able to affect the behavior of the cells involved: a) the different concentrations of reactive species, b) the intrinsic state of the target cells, as well as c) the presence of different growth factors, cytokines, and other mediators in the extracellular microenvironment or of other cellular sources of ROS.
Keywords	chemokines ; fibrosis ; liver ; liver diseases ; oxidative stress ; phenotype ; reactive oxygen species
Language	English
Dates of publication	2022-0628
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11071278
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The protease activated receptor 2 - CCAAT/enhancer-binding protein beta - SerpinB3 axis inhibition as a novel strategy for the treatment of non-alcoholic steatohepatitis.

Villano, Gianmarco / Novo, Erica / Turato, Cristian / Quarta, Santina / Ruvoletto, Mariagrazia / Biasiolo, Alessandra / Protopapa, Francesca / Chinellato, Monica / Martini, Andrea / Trevellin, Elisabetta / Granzotto, Marnie / Cannito, Stefania / Cendron, Laura / De Siervi, Silvia / Guido, Maria / Parola, Maurizio / Vettor, Roberto / Pontisso, Patrizia

Molecular metabolism

2024 Volume 81, Page(s) 101889

Abstract: Objective: The serine protease inhibitor SerpinB3 has been described as critical mediator of liver fibrosis and it has been recently proposed as an additional hepatokine involved in NASH development and insulin resistance. Protease Activated Receptor 2 ... ...

Abstract	Objective: The serine protease inhibitor SerpinB3 has been described as critical mediator of liver fibrosis and it has been recently proposed as an additional hepatokine involved in NASH development and insulin resistance. Protease Activated Receptor 2 has been identified as a novel regulator of hepatic metabolism. A targeted therapeutic strategy for NASH has been investigated, using 1-Piperidine Propionic Acid (1-PPA), since this compound has been recently proposed as both Protease Activated Receptor 2 and SerpinB3 inhibitor. Methods: The effect of SerpinB3 on inflammation and fibrosis genes was assessed in human macrophage and stellate cell lines. Transgenic mice, either overexpressing SerpinB3 or carrying Serpinb3 deletion and their relative wild type strains, were used in experimental NASH models. Subgroups of SerpinB3 transgenic mice and their controls were also injected with 1-PPA to assess the efficacy of this compound in NASH inhibition. Results: 1-PPA did not present significant cell and organ toxicity and was able to inhibit SerpinB3 and PAR2 in a dose-dependent manner. This effect was associated to a parallel reduction of the synthesis of the molecules induced by endogenous SerpinB3 or by its paracrine effects both in vitro and in vivo, leading to inhibition of lipid accumulation, inflammation and fibrosis in experimental NASH. At mechanistic level, the antiprotease activity of SerpinB3 was found essential for PAR2 activation, determining upregulation of the CCAAT Enhancer Binding Protein beta (C/EBP-β), another pivotal regulator of metabolism, inflammation and fibrosis, which in turn determined SerpinB3 synthesis. Conclusions: 1-PPA treatment was able to inhibit the PAR2 - C/EBP-β - SerpinB3 axis and to protect from NASH development and progression, supporting the potential use of a similar approach for a targeted therapy of NASH.
MeSH term(s)	Mice ; Animals ; Humans ; Non-alcoholic Fatty Liver Disease/metabolism ; Receptor, PAR-2 ; CCAAT-Enhancer-Binding Protein-beta ; Liver Cirrhosis/drug therapy ; Mice, Transgenic ; Inflammation
Chemical Substances	Receptor, PAR-2 ; CCAAT-Enhancer-Binding Protein-beta
Language	English
Publishing date	2024-02-01
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2024.101889
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Article ; Online: Hypoxia, Hypoxia-Inducible Factors and Liver Fibrosis

Beatrice Foglia / Erica Novo / Francesca Protopapa / Marina Maggiora / Claudia Bocca / Stefania Cannito / Maurizio Parola

Cells, Vol 10, Iss 1764, p

2021 Volume 1764

Abstract	Liver fibrosis is a potentially reversible pathophysiological event, leading to excess deposition of extracellular matrix (ECM) components and taking place as the net result of liver fibrogenesis, a dynamic and highly integrated process occurring during chronic liver injury of any etiology. Liver fibrogenesis and fibrosis, together with chronic inflammatory response, are primarily involved in the progression of chronic liver diseases (CLD). As is well known, a major role in fibrogenesis and fibrosis is played by activated myofibroblasts (MFs), as well as by macrophages and other hepatic cell populations involved in CLD progression. In the present review, we will focus the attention on the emerging pathogenic role of hypoxia, hypoxia-inducible factors (HIFs) and related mediators in the fibrogenic progression of CLD.
Keywords	hypoxia ; hypoxia-inducible factors ; liver fibrosis ; liver fibrogenesis ; chronic liver diseases ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Liver fibrogenesis: un update on established and emerging basic concepts

Novo, Erica / Bocca, Claudia / Foglia, Beatrice / Protopapa, Francesca / Maggiora, Marina / Parola, Maurizio / Cannito, Stefania

Archives of biochemistry and biophysics. 2020 Aug. 15, v. 689

2020

Abstract: Liver fibrogenesis is defined as a dynamic and highly integrated process occurring during chronic injury to liver parenchyma that can result in excess deposition of extracellular matrix (ECM) components (i.e., liver fibrosis). Liver fibrogenesis, ... ...

Abstract	Liver fibrogenesis is defined as a dynamic and highly integrated process occurring during chronic injury to liver parenchyma that can result in excess deposition of extracellular matrix (ECM) components (i.e., liver fibrosis). Liver fibrogenesis, together with chronic inflammatory response, is then primarily involved in the progression of chronic liver diseases (CLD) irrespective of the specific etiology. In the present review we will first offer a synthetic and updated overview of major basic concepts in relation to the role of myofibroblasts (MFs), macrophages and other hepatic cell populations involved in CLD to then offer an overview of established and emerging issues and mechanisms that have been proposed to favor and/or promote CLD progression. A special focus will be dedicated to selected issues that include emerging features in the field of cholangiopathies, the emerging role of genetic and epigenetic factors as well as of hypoxia, hypoxia-inducible factors (HIFs) and related mediators.
Keywords	biochemistry ; biophysics ; epigenetics ; etiology ; extracellular matrix ; hypoxia ; inflammation ; liver ; liver cirrhosis ; macrophages ; parenchyma (animal tissue)
Language	English
Dates of publication	2020-0815
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2020.108445
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: ERK Pathway in Activated, Myofibroblast-Like, Hepatic Stellate Cells: A Critical Signaling Crossroad Sustaining Liver Fibrosis.

Foglia, Beatrice / Cannito, Stefania / Bocca, Claudia / Parola, Maurizio / Novo, Erica

International journal of molecular sciences

2019 Volume 20, Issue 11

Abstract: Fibrogenic progression of chronic liver disease, whatever the etiology, is characterized by persistent chronic parenchymal injury, chronic activation of inflammatory response, and sustained activation of liver fibrogenesis, and of pathological wound ... ...

Abstract	Fibrogenic progression of chronic liver disease, whatever the etiology, is characterized by persistent chronic parenchymal injury, chronic activation of inflammatory response, and sustained activation of liver fibrogenesis, and of pathological wound healing response. A critical role in liver fibrogenesis is played by hepatic myofibroblasts (MFs), a heterogeneous population of α smooth-muscle actin-positive cells that originate from various precursor cells through a process of activation and transdifferentiation. In this review, we focus the attention on the role of extracellular signal-regulated kinase (ERK) signaling pathway as a critical one in modulating selected profibrogenic phenotypic responses operated by liver MFs. We will also analyze major therapeutic antifibrotic strategies developed in the last two decades in preclinical studies, some translated to clinical conditions, designed to interfere directly or indirectly with the Ras/Raf/MEK/ERK signaling pathway in activated hepatic MFs, but that also significantly increased our knowledge on the biology and pathobiology of these fascinating profibrogenic cells.
MeSH term(s)	Animals ; Biomarkers ; Cell Communication ; Cell Movement ; Cell Proliferation ; Cell Survival ; Combined Modality Therapy ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hepatic Stellate Cells/metabolism ; Humans ; Immunomodulation ; Liver Cirrhosis/etiology ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Liver Cirrhosis/therapy ; MAP Kinase Signaling System ; Molecular Targeted Therapy ; Myofibroblasts/metabolism ; Phenotype ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Biomarkers ; Reactive Oxygen Species ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2019-06-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20112700
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Article ; Online: Liver fibrogenesis: un update on established and emerging basic concepts.

Novo, Erica / Bocca, Claudia / Foglia, Beatrice / Protopapa, Francesca / Maggiora, Marina / Parola, Maurizio / Cannito, Stefania

Archives of biochemistry and biophysics

2020 Volume 689, Page(s) 108445

Abstract	Liver fibrogenesis is defined as a dynamic and highly integrated process occurring during chronic injury to liver parenchyma that can result in excess deposition of extracellular matrix (ECM) components (i.e., liver fibrosis). Liver fibrogenesis, together with chronic inflammatory response, is then primarily involved in the progression of chronic liver diseases (CLD) irrespective of the specific etiology. In the present review we will first offer a synthetic and updated overview of major basic concepts in relation to the role of myofibroblasts (MFs), macrophages and other hepatic cell populations involved in CLD to then offer an overview of established and emerging issues and mechanisms that have been proposed to favor and/or promote CLD progression. A special focus will be dedicated to selected issues that include emerging features in the field of cholangiopathies, the emerging role of genetic and epigenetic factors as well as of hypoxia, hypoxia-inducible factors (HIFs) and related mediators.
MeSH term(s)	Animals ; Chronic Disease ; Disease Progression ; Epigenesis, Genetic ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Macrophages/metabolism ; Macrophages/pathology ; Myofibroblasts/metabolism ; Myofibroblasts/pathology
Language	English
Publishing date	2020-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2020.108445
Database	MEDical Literature Analysis and Retrieval System OnLINE

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