Hepatic Fibrosis: From Pathogenesis to Clinical Management

A special issue of Livers (ISSN 2673-4389).

Deadline for manuscript submissions: closed (20 October 2021) | Viewed by 15236

Special Issue Editor

Special Issue Information

Dear Colleagues,

Liver fibrosis is a major challenge of global health. It occurs after repetitive or long-lasting injury to the liver and is characterized by excessive formation and deposition of fibrous connective tissue and architectural tissue remodeling. Although the molecular and cellular mechanisms contributing to the pathogenesis of liver fibrosis are well understood, pharmacological intervention targeting its progression is complicated and often only effective in experimental models. In this Special issue of Livers, I invite you to contribute original and cutting-edge research articles, reviews, shorter perspectives, or letters related to the theme of “Hepatic Fibrosis: From Pathogenesis to Clinical Management”.

In particular, expert articles reporting new mechanistic or general aspects of hepatic fibrogenesis are highly welcome. Relevant topics include but are not limited to: extracellular matrix, fibrotic signaling, immunomodulation, novel or improved experimental models, relevant cytokines/chemokines, inflammatory triggers, NASH, NAFLD, ASH, hepatitis, genetic predisposition, microbiota, bioimaging, therapeutic perspectives, and translational aspects.

Prof. Dr. Ralf Weiskirchen
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Livers is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Liver fibrosis
  • Hepatic stellate cells/myofibroblasts
  • NASH/NAFLD/ASH
  • Extracellular matrix
  • Cholestasis
  • Hepatitis
  • Bile salts
  • Inflammation
  • Cytokines/chemokines
  • Therapy

Published Papers (3 papers)

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Research

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13 pages, 4835 KiB  
Article
Effects of Ethanol Feeding in Early-Stage NAFLD Mice Induced by Western Diet
by Maximilian Joseph Brol, Stella Georgiou, Ditlev Nytoft Rasmussen, Cristina Ortiz, Sabine Klein, Robert Schierwagen, Frank Erhard Uschner, Larissa Eberle, Sönke Detlefsen, Vasiliki I. Pantazopoulou, Maja Thiele, Vasiliki Filippa, Sandra Torres, Ema Anastasiadou, Aleksander Krag and Jonel Trebicka
Livers 2021, 1(1), 27-39; https://doi.org/10.3390/livers1010003 - 21 Feb 2021
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Abstract
Background: The prevalence of metabolic liver diseases is increasing and approved pharmacological treatments are still missing. Many animal models of nonalcoholic fatty liver disease (NAFLD) show a full spectrum of fibrosis, inflammation and steatosis, which does not reflect the human situation since [...] Read more.
Background: The prevalence of metabolic liver diseases is increasing and approved pharmacological treatments are still missing. Many animal models of nonalcoholic fatty liver disease (NAFLD) show a full spectrum of fibrosis, inflammation and steatosis, which does not reflect the human situation since only up to one third of the patients develop fibrosis and nonalcoholic steatohepatitis (NASH). Methods: Seven week old C57Bl/J mice were treated with ethanol, Western diet (WD) or both. The animals’ liver phenotypes were determined through histology, immunohistochemistry, Western blotting, hepatic triglyceride content and gene expression levels. In a human cohort of 80 patients stratified by current alcohol misuse and body mass index, liver histology and gene expression analysis were performed. Results: WD diet and ethanol-treated animals showed severe steatosis, with high hepatic triglyceride content and upregulation of fatty acid synthesis. Mild fibrosis was revealed using Sirius-red stains and gene expression levels of collagen. Inflammation was detected using histology, immunohistochemistry and upregulation of proinflammatory genes. The human cohort of obese drinkers showed similar upregulation in genes related to steatosis, fibrosis and inflammation. Conclusions: We provide a novel murine model for early-stage fatty liver disease suitable for drug testing and investigation of pathophysiology. Full article
(This article belongs to the Special Issue Hepatic Fibrosis: From Pathogenesis to Clinical Management)
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Review

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33 pages, 2191 KiB  
Review
Targeting Gut–Liver Axis for Treatment of Liver Fibrosis and Portal Hypertension
by Eric Kalo, Scott Read and Golo Ahlenstiel
Livers 2021, 1(3), 147-179; https://doi.org/10.3390/livers1030014 - 09 Sep 2021
Cited by 3 | Viewed by 7533
Abstract
Antifibrotic therapies for the treatment of liver fibrosis represent an unconquered area of drug development. The significant involvement of the gut microbiota as a driving force in a multitude of liver disease, be it pathogenesis or fibrotic progression, suggest that targeting the gut–liver [...] Read more.
Antifibrotic therapies for the treatment of liver fibrosis represent an unconquered area of drug development. The significant involvement of the gut microbiota as a driving force in a multitude of liver disease, be it pathogenesis or fibrotic progression, suggest that targeting the gut–liver axis, relevant signaling pathways, and/or manipulation of the gut’s commensal microbial composition and its metabolites may offer opportunities for biomarker discovery, novel therapies and personalized medicine development. Here, we review potential links between bacterial translocation and deficits of host-microbiome compartmentalization and liver fibrosis that occur in settings of advanced chronic liver disease. We discuss established and emerging therapeutic strategies, translated from our current knowledge of the gut–liver axis, targeted at restoring intestinal eubiosis, ameliorating hepatic fibrosis and rising portal hypertension that characterize and define the course of decompensated cirrhosis. Full article
(This article belongs to the Special Issue Hepatic Fibrosis: From Pathogenesis to Clinical Management)
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Other

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4 pages, 405 KiB  
Comment
The Cape Gooseberry Constituent Physalin B Ameliorates Nonalcoholic Steatohepatitis and Attenuates Liver Fibrosis
by Sabine Weiskirchen and Ralf Weiskirchen
Livers 2021, 1(2), 98-101; https://doi.org/10.3390/livers1020009 - 02 Jun 2021
Viewed by 3059
Abstract
Physalin B belongs to a family of Physalins that can be isolated from the genus Physalis (Solanaceae). In traditional Chinese Medicine, Physalis angulata L. is frequently used to treat a variety of illnesses such as dermatitis, trachitis, rheumatism, and hepatitis. Physalin [...] Read more.
Physalin B belongs to a family of Physalins that can be isolated from the genus Physalis (Solanaceae). In traditional Chinese Medicine, Physalis angulata L. is frequently used to treat a variety of illnesses such as dermatitis, trachitis, rheumatism, and hepatitis. Physalin B promotes cellular apoptosis and has antitumor, antimalarial, and antimycobacterial activities. Two recent studies evaluated the therapeutic activities of Physalin B in pre-clinical hepatic disease models. In this comment, a brief summary of the most important findings of these two studies is given and discussed. Full article
(This article belongs to the Special Issue Hepatic Fibrosis: From Pathogenesis to Clinical Management)
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