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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: 31 May 2025 | Viewed by 7956

Special Issue Editors

Prof. Dr. Ralf Weiskirchen

grade 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 (7 papers)

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Editorial

Jump to: Research, Review, Other

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 1244
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, Other

27 pages, 9450 KiB  
Article
Innovative Elastography Measuring Cap for Ex Vivo Liver Condition Assessment: Numerical and Preclinical Studies in a Porcine Model
by Dariusz Pyka, Agnieszka Noszczyk-Nowak, Karina Krawiec, Tomasz Świetlik and Krzysztof J. Opieliński
Livers 2025, 5(1), 3; https://doi.org/10.3390/livers5010003 - 16 Jan 2025
Viewed by 448
Abstract
The authors of this study focused their research on developing cap geometries for the FibroScan® elastograph (FibroScan, EchoSens, Paris, France) measuring head aimed at a non-invasive assessment of liver condition for transplantation using a pig animal model. Numerical models were created to [...] Read more.
The authors of this study focused their research on developing cap geometries for the FibroScan® elastograph (FibroScan, EchoSens, Paris, France) measuring head aimed at a non-invasive assessment of liver condition for transplantation using a pig animal model. Numerical models were created to simulate the propagation of a mechanical wave through a biological medium induced by the FibroScan® elastograph measuring head. The designed caps were intended to replicate the skin–muscle–rib–liver structures to minimize the risk of damage caused by mechanical wave excitation when directly applied to liver tissue. The construction process of numerical models for the liver and surrounding tissues is presented, along with simulations reflecting the mechanical and acoustic properties of the wave propagation process. The results obtained from in vivo measurements on pigs were validated through a numerical analysis, confirming a high level of agreement between the test results and the numerical model. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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18 pages, 2510 KiB  
Article
Advancing Chronic Liver Disease Diagnoses: Targeted Proteomics for the Non-Invasive Detection of Fibrosis
by Andrea Villanueva Raisman, David Kotol, Ozlem Altay, Adil Mardinoglu, Dila Atak, Cihan Yurdaydin, Murat Akyildiz, Murat Dayangac, Hale Kirimlioglu, Müjdat Zeybel and Fredrik Edfors
Livers 2025, 5(1), 2; https://doi.org/10.3390/livers5010002 - 14 Jan 2025
Viewed by 625
Abstract
Chronic liver disease poses significant challenges to healthcare systems, which frequently struggle to meet the needs of end-stage liver disease patients. Early detection and management are essential because liver damage and fibrosis are potentially reversible. However, the implementation of population-wide screenings is hindered [...] Read more.
Chronic liver disease poses significant challenges to healthcare systems, which frequently struggle to meet the needs of end-stage liver disease patients. Early detection and management are essential because liver damage and fibrosis are potentially reversible. However, the implementation of population-wide screenings is hindered by the asymptomatic nature of early chronic liver disease, along with the risks and costs associated with traditional diagnostics, such as liver biopsies. This study pioneers the development of innovative, minimally invasive methods capable of improving the outcomes of liver disease patients by identifying liver disease biomarkers using quantification methods with translational potential. A targeted mass spectrometry assay based on stable isotope standard protein epitope signature tags (SIS-PrESTs) was employed for the absolute quantification of 108 proteins in just two microliters of plasma. The plasma profiles were derived from patients of various liver disease stages and etiologies, including healthy controls. A set of potential biomarkers for stratifying liver fibrosis was identified through differential expression analysis and supervised machine learning. These findings offer promising alternatives for improved diagnostics and personalized treatment strategies in liver disease management. Moreover, our approach is fully compatible with existing technologies that facilitate the robust quantification of clinically relevant protein targets via minimally disruptive sampling methods. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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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 778
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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58 pages, 1608 KiB  
Review
Immune Checkpoints and the Immunology of Liver Fibrosis
by Ioannis Tsomidis, Argyro Voumvouraki and Elias Kouroumalis
Livers 2025, 5(1), 5; https://doi.org/10.3390/livers5010005 - 27 Jan 2025
Viewed by 502
Abstract
Liver fibrosis is a very complicated dynamic process where several immune cells are involved. Both innate and adaptive immunity are implicated, and their interplay is always present. Multi-directional interactions between liver macrophages, hepatic stellate cells (HSCs), immune cells, and several cytokines are important [...] Read more.
Liver fibrosis is a very complicated dynamic process where several immune cells are involved. Both innate and adaptive immunity are implicated, and their interplay is always present. Multi-directional interactions between liver macrophages, hepatic stellate cells (HSCs), immune cells, and several cytokines are important for the induction and perpetuation of liver fibrosis. Detailed studies of proteomics and transcriptomics have produced new evidence for the role of individual cells in the process of liver fibrosis and cirrhosis. Most of these cells are controlled by the various immune checkpoints whose main function is to maintain the homeostasis of the implicated immune cells. Recent evidence indicates that several immune checkpoints are involved in liver fibrosis. In particular, the role of the programmed cell death protein 1 (PD-1), the programmed death-ligand 1 (PD-L1), and the role of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) have been investigated, particularly after the availability of checkpoint inhibitors. Their activation leads to the exhaustion of CD4+ve and CD8+ve T cells and the promotion of liver fibrosis. In this review, the current pathogenesis of liver fibrosis and the immunological abnormalities are discussed. The recent data on the involvement of immune checkpoints are identified as possible targets of future interventions. Full article
(This article belongs to the Special Issue Liver Fibrosis: Mechanisms, Targets, Assessment and Treatment)
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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 5 | Viewed by 1943
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 637
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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