Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 2329

Special Issue Editors


E-Mail Website
Guest Editor
Department of Internal Medicine I, University Hospital of Bonn, 53127 Bonn, Germany
Interests: portal hypertension; bile acids; beta-blockers; NASH; NAFLD; cirrhosis; therapy

Special Issue Information

Dear Colleagues,

Fibrosis is a double-edged sword. On the one hand, it can be the final state of healed inflammation as scar tissue; on the other hand, it is frequently associated with a reduction in or loss of organ function. Moreover, especially in liver disease, it is a surrogate parameter that indicates the progression of the disease to liver cirrhosis or even hepatocellular carcinoma. This is especially true for non-alcoholic fatty liver disease, a pandemic disorder associated with Western lifestyles and diets. To influence organ fibrosis, it is important to better understand its induction, perpetuation and termination at the molecular level. The induction of liver fibrosis may be metabolic (e.g., alcohol, diet and drugs), infectious (e.g., viruses), autoimmune (e.g., primary biliary cholangitis) or due to monogenetic defects (e.g., increased iron storage). The molecular mechanisms leading to final-stage fibrosis are very different—dependent on its pathogenesis. It is the aim of this Special Issue to provide more insight into these processes.

Prof. Dr. Ralf Weiskirchen
Prof. Dr. Tilman Sauerbruch
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • fibrosis
  • hepatic stellate cells
  • portal hypertension
  • extracellular matrix
  • cytokines
  • chemokines
  • biomarkers
  • NASH
  • NAFLD
  • cirrhosis
  • hepatocellular carcinoma
  • therapy
  • animal models
  • imaging of hepatic fibrosis
  • biomarkers of hepatic fibrosis

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Editorial

Jump to: Review

3 pages, 890 KiB  
Editorial
Special Issue “Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment”
by Ralf Weiskirchen and Tilman Sauerbruch
Livers 2023, 3(3), 322-324; https://doi.org/10.3390/livers3030023 - 27 Jun 2023
Viewed by 775
Abstract
Fibrosis is a double-edged sword [...] Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
Show Figures

Figure 1

Review

Jump to: Editorial

14 pages, 2067 KiB  
Review
The Pivotal Role of the Membrane-Bound O-Acyltransferase Domain Containing 7 in Non-Alcoholic Fatty Liver Disease
by Preethi Chandrasekaran and Ralf Weiskirchen
Livers 2024, 4(1), 1-14; https://doi.org/10.3390/livers4010001 - 20 Dec 2023
Viewed by 920
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common and prevalent disorder affecting 25 percent of the adults in the United States and 32 percent of adults globally. It is one of the common causes of chronic liver disease characterized by steatosis, which can [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is a common and prevalent disorder affecting 25 percent of the adults in the United States and 32 percent of adults globally. It is one of the common causes of chronic liver disease characterized by steatosis, which can lead to inflammation, fibrosis, and cirrhosis. NAFLD is strongly associated with obesity and insulin resistance. Multiple genetic variants have been consistently found to be associated with NAFLD; one of them is found in the TMC4-MBOAT7 loci. One variant (rs641738 C>T) within MBOAT7 encoding lysophosphatidyl inositol acyltransferase increases the risk for NAFLD development and triggers hepatic inflammation by regulating arachidonic acid levels. This review provides an overview of the MBOAT7 gene, pathogenesis of NAFLD, understanding the regulation of MBOAT7 and mechanistic link between MBOAT7 and NAFLD. It further summarizes pathophysiologically relevant in vivo and in vitro studies on MBOAT7 and challenges in treating complex NAFLD with recent progress made in the treatment of NAFLD. As such, this review provides useful information on MBOAT7 and NAFLD interrelation, which has the potential of deciphering novel therapeutic targets rather than well-known genetic variants such as PNPLA3 and TM6SF2. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
Show Figures

Graphical abstract

Back to TopTop