Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 5270

Special Issue Editors


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Guest Editor

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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

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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 (4 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 1139
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

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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 657
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 1731
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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Other

8 pages, 581 KiB  
Case Report
Progressive Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) from a Young Age Due to a Rare Genetic Disorder, Familial Partial Lipodystrophy: A Case Report and Review of the Literature
by Elena Vorona, Ekaterina Sorkina and Jonel Trebicka
Livers 2024, 4(4), 688-695; https://doi.org/10.3390/livers4040047 - 13 Dec 2024
Viewed by 223
Abstract
Steatotic liver disease is common in the general population and is associated with higher risk for cardiovascular diseases. Early diagnosis and appropriate therapy can prevent the development of irreversible end-stage liver fibrosis and reduce liver-related and cardiovascular mortality. It is important to recognise [...] Read more.
Steatotic liver disease is common in the general population and is associated with higher risk for cardiovascular diseases. Early diagnosis and appropriate therapy can prevent the development of irreversible end-stage liver fibrosis and reduce liver-related and cardiovascular mortality. It is important to recognise not only the common causes of metabolic dysfunction-associated steatotic liver disease, such as type 2 diabetes mellitus or morbid obesity, but also rare conditions, because their treatment is different from conventional therapy. Here, we report a female patient with familial partial lipodystrophy, in whom the diagnosis was not confirmed until several years after the initial manifestation, which delayed the start of pathogenetic therapy. After the initiation of leptin replacement therapy, a significant improvement in liver stiffness measurement was achieved within a few months. In addition, we summarise the current treatment options for diabetes and their influence on steatosis hepatis. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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