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Livers
Special Issues
Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment
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Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 4728

Special Issue Editors

Prof. Dr. Ralf Weiskirchen

E-Mail Website
Guest Editor
Head of the Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), RWTH University Hospital Aachen, Aachen, Germany
Interests: liver fibrosis; liver cell subpopulations; organoids; animal models; TGF-β; PDGF; metals; mass spectrometry; biomarkers
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Tilman Sauerbruch

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

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Published Papers (3 papers)

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Editorial

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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 1083
Abstract
Fibrosis is a double-edged sword [...] Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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Research

Jump to: Editorial, Review

12 pages, 1549 KiB  
Article
Useful Predictor for Exacerbation of Esophagogastric Varices after Hepatitis C Virus Eradication by Direct-Acting Antivirals
by Yuko Nagaoki, Kenji Yamaoka, Yasutoshi Fujii, Shinsuke Uchikawa, Hatsue Fujino, Atsushi Ono, Eisuke Murakami, Tomokazu Kawaoka, Daiki Miki, Hiroshi Aikata, C. Nelson Hayes, Masataka Tsuge and Shiro Oka
Livers 2024, 4(3), 352-363; https://doi.org/10.3390/livers4030025 - 30 Jul 2024
Viewed by 590
Abstract
To clarify the risk factors for the aggravation of esophagogastric varices (EGVs) after hepatitis C virus (HCV) eradication with direct-acting antiviral (DAA) therapy, we enrolled 167 consecutive patients with HCV-related compensated cirrhosis who achieved a sustained virological response (SVR) after DAA therapy. During [...] Read more.
To clarify the risk factors for the aggravation of esophagogastric varices (EGVs) after hepatitis C virus (HCV) eradication with direct-acting antiviral (DAA) therapy, we enrolled 167 consecutive patients with HCV-related compensated cirrhosis who achieved a sustained virological response (SVR) after DAA therapy. During a median of 69 months, EGVs were aggravated in 42 (25%) patients despite SVR. The cumulative 1-, 3-, 5-, and 10-year aggravated EGV rates were 7%, 23%, 25%, and 27%, respectively. Multivariate analysis identified a platelet count < 11.0 × 104/μL, LSM ≥ 18.0 kPa, total bile acid ≥ 33.0 μmol/L, and a diameter of left gastric vein (LGV) ≥ 5.0 mm at HCV eradication as independent risk factors for EGV aggravation post-SVR. In groups that met all of these risks, the cumulative EGV aggravation rates at 1, 3, and 5 years were 27%, 87%, and 91%, respectively. However, none of the patients who had only one or none of the risk factors experienced EGV aggravation. Platelet count, LSM, total bile acid, and diameter of LGV at HCV eradication were associated with aggravated EGV post-SVR. EGVs tend to worsen as two or more of these risk factors increase. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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Review

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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
Cited by 3 | Viewed by 1624
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)
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