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Record Nr. |
UNINA9910814001803321 |
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Titolo |
Stellate cells in health and disease / / edited by Chandrashekhar R. Gandhi, Massimo Pinzani |
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Pubbl/distr/stampa |
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Amsterdam, [Netherlands] : , : Academic Press, , 2015 |
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©2015 |
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Descrizione fisica |
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1 online resource (335 p.) |
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Disciplina |
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Soggetti |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Note generali |
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Description based upon print version of record. |
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Nota di bibliografia |
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Includes bibliographical references at the end of each chapters and index. |
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Nota di contenuto |
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Front Cover; Stellate Cells in Health and Disease; Copyright Page; Dedication; Contents; List of Contributors; Foreword; What have we learned?; The outlook for anti-fibrotic treatment; References; Preface; 1 History and Early Work; 1.1 Discovery of Hepatic Stellate Cells; 1.2 HSCs and Vitamin A Homeostasis; 1.3 Morphological Characteristics of HSCs; 1.4 HSCs and Liver Fibrosis; 1.5 Isolation and Culture of HSCs; 1.6 Activation and Transdifferentiation of HSCs; 1.7 Markers for HSCs; 1.8 Perspective; References; 2 Hepatic Stellate Cell Culture Models; 2.1 Isolation of Hepatic Stellate Cells |
2.2 Single Cell Culture2.3 In Vitro- Versus In Vivo-Activated HSCs; 2.4 Single Cell Culture and 2D: Importance of Adhesion, Arg-Gly-Asp, and Matrix Components; 2.5 HSC Co-Cultures with Kupffer Cells, Hepatocytes, LSEC, HCC, and CC Cells; 2.6 In Vitro 3D Culture Systems; 2.7 Conclusions; References; 3 Hepatic Fibrosis: A Global Clinical Problem; 3.1 Introduction; 3.2 Chronic Viral Hepatitis; 3.2.1 Alcohol-induced liver fibrosis; 3.3 NAFLD and NASH; 3.4 Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Primary Sclerosing Cholangitis; 3.5 Etiology-Driven Liver Fibrosis; 3.5.1 Perspectives |
References4 Stellate Cells and Hepatic Fibrosis; 4.1 Introduction; 4.2 Pathogenesis of Hepatic Fibrosis; 4.2.1 Pathological and clinical associations of hepatic fibrosis; 4.2.2 ECM composition and matrix homeostasis; 4.2.3 Cellular sources of ECM; 4.3 HSCs and Hepatic |
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Fibrosis; 4.3.1 Initiation; 4.3.2 Perpetuation; 4.3.2.1 Retinoid loss; 4.3.2.2 Fibrogenesis; 4.3.2.3 Matrix turnover; 4.3.2.4 Chemotaxis; 4.3.2.5 Proliferation; 4.3.2.6 Contractility; 4.3.2.7 Immunoregulation; 4.3.3 Regression; 4.3.3.1 Apoptosis; 4.3.3.2 Senescence; 4.3.3.3 Reversion to an inactivated phenotype |
4.4 New and Emerging Pathways of HSC Activation4.5 Conclusions; References; 5 Cytokine Production and Signaling in Stellate Cells; 5.1 Introduction; 5.2 Platelet-Derived Growth Factor; 5.3 Angiogenic Cytokines; 5.4 TGF-β Superfamily; 5.5 Chemokines; 5.6 Tumor Necrosis Factor Superfamily; 5.7 Interleukins and Interferons; 5.8 Adipokines and Other Cytokines Related to Metabolism; 5.9 Osteopontin; 5.10 Perspective; References; 6 Stellate Cells, Portal Myofibroblasts, and Epithelial-to-Mesenchymal Transition; 6.1 Introduction; 6.2 Hepatic Stellate Cells |
6.2.1 Contribution of HSCs to liver fibrosis6.2.1.1 HSCs/Myofibroblasts are the primary target of anti-fibrotic therapy; 6.2.1.2 Reversibility of liver fibrosis; 6.2.1.3 Inactivation of HSCs (iHSCs); 6.2.2 Other functions of HSCs; 6.2.2.1 Distinct functions of senescent HSCs; 6.2.2.2 HSC as regulatory bystanders; 6.2.2.3 HSCs as regulators of hepatocellular damage; 6.2.2.4 The role of HSCs in liver regeneration; 6.3 Portal Fibroblasts; 6.3.1 Characterization of PFs; 6.4 Epithelial-to-Mesenchymal Transition; 6.5 Perspective; References; 7 Matrix Metalloproteinases and Their Inhibitors |
7.1 Introduction |
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