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Liver Diseases: From Bench to Bedside
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Liver Diseases: From Bench to Bedside

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 March 2024) | Viewed by 8751

Special Issue Editors

Dr. Tatsuo Kanda

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan
Interests: viral hepatitis; hepatocellular carcinoma; innate immunity; unfolded protein response
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Mitsuhiko Moriyama

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi-ku, Tokyo 173-8610, Japan
Interests: hepatitis; trace element; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In daily clinical practice, we see many patients with liver diseases and occasionally encounter difficulty in trying to cure their diseases. We may also run across interesting findings in patients with liver disease. At that time, we should perform research from the bedside to bench and try to discover useful and powerful methods to solve their problems. When we perform basic research with new technologies and modern techniques, we may accidentally find useful events for patients with liver disease. Conversely, we should apply them from bench to bedside. This Special Issue plans to provide an overview of the most recent advances in the field of liver disease and its related infectious diseases. We will return bench and bedside with the new normal and offer helpful treatment for patients.

Potential topics include, but are not limited to:

  • hepatology;
  • viral hepatitis;
  • mechanisms of action;
  • molecular research;
  • antivirals;
  • molecular targeting therapy;
  • immune checkpoint inhibitor;
  • immune-mediated adverse events imaging modality.

Dr. Tatsuo Kanda
Prof. Dr. Mitsuhiko Moriyama
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • hepatology
  • viral hepatitis
  • hepatocellular carcinoma
  • liver cancer
  • cirrhosis
  • hepatic fibrosis
  • HAV
  • HEV

Published Papers (5 papers)

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Research

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19 pages, 3741 KiB  
Article
Serological and Molecular Characterization of Hepatitis C Virus-Related Cryoglobulinemic Vasculitis in Patients without Cryoprecipitate
by Cecilia Napodano, Gabriele Ciasca, Patrizia Chiusolo, Krizia Pocino, Laura Gragnani, Annunziata Stefanile, Francesca Gulli, Serena Lorini, Gessica Minnella, Federica Fosso, Riccardo Di Santo, Sabrina Romanò, Valerio Basile, Valerio De Stefano, Gian Ludovico Rapaccini, Anna Linda Zignego, Enrico Di Stasio, Mariapaola Marino and Umberto Basile
Int. J. Mol. Sci. 2023, 24(14), 11602; https://doi.org/10.3390/ijms241411602 - 18 Jul 2023
Cited by 2 | Viewed by 1111
Abstract
Prolonged B cells stimulation due to the Hepatitis C virus (HCV) can result in autoimmunity, stigmatized by rising levels of cryoglobulins (CGs), the rheumatoid factor (RF), and free light chains (FLC) of immunoglobulins (Ig) associated with a range of symptoms, from their absence [...] Read more.
Prolonged B cells stimulation due to the Hepatitis C virus (HCV) can result in autoimmunity, stigmatized by rising levels of cryoglobulins (CGs), the rheumatoid factor (RF), and free light chains (FLC) of immunoglobulins (Ig) associated with a range of symptoms, from their absence to severe cryoglobulinemic vasculitis and lymphoma. Here, we aimed to identify an immunological signature for the earliest stages of vasculitis when cryoprecipitate is still not detectable. We firstly analyzed the IgG subclasses, FLC, and RF in 120 HCV-RNA-positive patients divided into four groups according to the type of cryoprecipitate and symptoms: 30 asymptomatic without cryoprecipitate (No Cryo), 30 with vasculitis symptoms but without CGs that we supposed were circulating but still not detectable (Circulating), 30 type II and 30 type III mixed cryoglobulinemia (Cryo II and Cryo III, respectively). Our results revealed that patients with supposed circulating CGs displayed a pattern of serological parameters that closely resembled Cryo II and Cryo III, with a stronger similarity to Cryo II. Accordingly, we analyzed the groups of Circulating and Cryo II for their immunoglobulin heavy chain (IgH) and T-cell receptor (TCR) gene rearrangements, finding a similar mixed distribution of monoclonal, oligoclonal, and polyclonal responses compared to a control group of ten HCV-RNA-negative patients recovered from infection, who displayed a 100% polyclonal response. Our results strengthened the hypothesis that circulating CGs are the origin of symptoms in HCV-RNA-positive patients without cryoprecipitate and demonstrated that an analysis of clonal IGH and TCR rearrangements is the best option for the early diagnosis of extrahepatic complications. Full article
(This article belongs to the Special Issue Liver Diseases: From Bench to Bedside)
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14 pages, 1734 KiB  
Article
Masitinib Inhibits Hepatitis A Virus Replication
by Reina Sasaki-Tanaka, Toshikatsu Shibata, Mitsuhiko Moriyama, Hirofumi Kogure, Asuka Hirai-Yuki, Hiroaki Okamoto and Tatsuo Kanda
Int. J. Mol. Sci. 2023, 24(11), 9708; https://doi.org/10.3390/ijms24119708 - 03 Jun 2023
Cited by 1 | Viewed by 2435
Abstract
The hepatitis A virus (HAV) infection causes acute hepatitis. HAV also induces acute liver failure or acute-on-chronic liver failure; however, no potent anti-HAV drugs are currently available in clinical situations. For anti-HAV drug screening, more convenient and useful models that mimic HAV replication [...] Read more.
The hepatitis A virus (HAV) infection causes acute hepatitis. HAV also induces acute liver failure or acute-on-chronic liver failure; however, no potent anti-HAV drugs are currently available in clinical situations. For anti-HAV drug screening, more convenient and useful models that mimic HAV replication are needed. In the present study, we established HuhT7-HAV/Luc cells, which are HuhT7 cells stably expressing the HAV HM175-18f genotype IB subgenomic replicon RNA harboring the firefly luciferase gene. This system was made by using a PiggyBac-based gene transfer system that introduces nonviral transposon DNA into mammalian cells. Then, we investigated whether 1134 US Food and Drug Administration (FDA)-approved drugs exhibited in vitro anti-HAV activity. We further demonstrated that treatment with tyrosine kinase inhibitor masitinib significantly reduced both HAV HM175-18f genotype IB replication and HAV HA11-1299 genotype IIIA replication. Masitinib also significantly inhibited HAV HM175 internal ribosomal entry-site (IRES) activity. In conclusion, HuhT7-HAV/Luc cells are adequate for anti-HAV drug screening, and masitinib may be useful for the treatment of severe HAV infection. Full article
(This article belongs to the Special Issue Liver Diseases: From Bench to Bedside)
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13 pages, 1164 KiB  
Article
Gut-Microbiota Dysbiosis in Stroke-Prone Spontaneously Hypertensive Rats with Diet-Induced Steatohepatitis
by Shini Kanezawa, Mitsuhiko Moriyama, Tatsuo Kanda, Akiko Fukushima, Ryota Masuzaki, Reina Sasaki-Tanaka, Akiko Tsunemi, Takahiro Ueno, Noboru Fukuda and Hirofumi Kogure
Int. J. Mol. Sci. 2023, 24(5), 4603; https://doi.org/10.3390/ijms24054603 - 27 Feb 2023
Cited by 1 | Viewed by 2006
Abstract
Metabolic-dysfunction-associated fatty-liver disease (MAFLD) is the principal worldwide cause of liver disease. Individuals with nonalcoholic steatohepatitis (NASH) have a higher prevalence of small-intestinal bacterial overgrowth (SIBO). We examined gut-microbiota isolated from 12-week-old stroke-prone spontaneously hypertensive-5 rats (SHRSP5) fed on a normal diet (ND) [...] Read more.
Metabolic-dysfunction-associated fatty-liver disease (MAFLD) is the principal worldwide cause of liver disease. Individuals with nonalcoholic steatohepatitis (NASH) have a higher prevalence of small-intestinal bacterial overgrowth (SIBO). We examined gut-microbiota isolated from 12-week-old stroke-prone spontaneously hypertensive-5 rats (SHRSP5) fed on a normal diet (ND) or a high-fat- and high-cholesterol-containing diet (HFCD) and clarified the differences between their gut-microbiota. We observed that the Firmicute/Bacteroidetes (F/B) ratio in both the small intestines and the feces of the SHRSP5 rats fed HFCD increased compared to that of the SHRSP5 rats fed ND. Notably, the quantities of the 16S rRNA genes in small intestines of the SHRSP5 rats fed HFCD were significantly lower than those of the SHRSP5 rats fed ND. As in SIBO syndrome, the SHRSP5 rats fed HFCD presented with diarrhea and body-weight loss with abnormal types of bacteria in the small intestine, although the number of bacteria in the small intestine did not increase. The microbiota of the feces in the SHRSP5 rats fed HFCD was different from those in the SHRP5 rats fed ND. In conclusion, there is an association between MAFLD and gut-microbiota alteration. Gut-microbiota alteration may be a therapeutic target for MAFLD. Full article
(This article belongs to the Special Issue Liver Diseases: From Bench to Bedside)
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Review

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20 pages, 723 KiB  
Review
Exploring Advanced Therapies for Primary Biliary Cholangitis: Insights from the Gut Microbiota–Bile Acid–Immunity Network
by Ziqi Guo, Kun He, Ke Pang, Daiyu Yang, Chengzhen Lyu, Haifeng Xu and Dong Wu
Int. J. Mol. Sci. 2024, 25(8), 4321; https://doi.org/10.3390/ijms25084321 - 13 Apr 2024
Viewed by 304
Abstract
Primary biliary cholangitis (PBC) is a cholestatic liver disease characterized by immune-mediated injury to small bile ducts. Although PBC is an autoimmune disease, the effectiveness of conventional immunosuppressive therapy is disappointing. Nearly 40% of PBC patients do not respond to the first-line drug [...] Read more.
Primary biliary cholangitis (PBC) is a cholestatic liver disease characterized by immune-mediated injury to small bile ducts. Although PBC is an autoimmune disease, the effectiveness of conventional immunosuppressive therapy is disappointing. Nearly 40% of PBC patients do not respond to the first-line drug UDCA. Without appropriate intervention, PBC patients eventually progress to liver cirrhosis and even death. There is an urgent need to develop new therapies. The gut–liver axis emphasizes the interconnection between the gut and the liver, and evidence is increasing that gut microbiota and bile acids play an important role in the pathogenesis of cholestatic diseases. Dysbiosis of gut microbiota, imbalance of bile acids, and immune-mediated bile duct injury constitute the triad of pathophysiology in PBC. Autoimmune cholangitis has the potential to be improved through immune system modulation. Considering the failure of conventional immunotherapies and the involvement of gut microbiota and bile acids in the pathogenesis, targeting immune factors associated with them, such as bile acid receptors, microbial-derived molecules, and related specific immune cells, may offer breakthroughs. Understanding the gut microbiota–bile acid network and related immune dysfunctions in PBC provides a new perspective on therapeutic strategies. Therefore, we summarize the latest advances in research of gut microbiota and bile acids in PBC and, for the first time, explore the possibility of related immune factors as novel immunotherapy targets. This article discusses potential therapeutic approaches focusing on regulating gut microbiota, maintaining bile acid homeostasis, their interactions, and related immune factors. Full article
(This article belongs to the Special Issue Liver Diseases: From Bench to Bedside)
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33 pages, 1123 KiB  
Review
Advanced Biomarkers of Hepatotoxicity in Psychiatry: A Narrative Review and Recommendations for New Psychoactive Substances
by Aniela Golub, Michal Ordak, Tadeusz Nasierowski and Magdalena Bujalska-Zadrozny
Int. J. Mol. Sci. 2023, 24(11), 9413; https://doi.org/10.3390/ijms24119413 - 28 May 2023
Cited by 1 | Viewed by 2247
Abstract
One of the factors that increase the effectiveness of the pharmacotherapy used in patients abusing various types of new psychoactive substances (NPSs) is the proper functioning of the liver. However, the articles published to date on NPS hepatotoxicity only address non-specific hepatic parameters. [...] Read more.
One of the factors that increase the effectiveness of the pharmacotherapy used in patients abusing various types of new psychoactive substances (NPSs) is the proper functioning of the liver. However, the articles published to date on NPS hepatotoxicity only address non-specific hepatic parameters. The aim of this manuscript was to review three advanced markers of hepatotoxicity in psychiatry, namely, osteopontin (OPN), high-mobility group box 1 protein (HMGB1) and glutathione dehydrogenase (GDH, GLDH), and, on this basis, to identify recommendations that should be included in future studies in patients abusing NPSs. This will make it possible to determine whether NPSs do indeed have a hepatotoxic effect or whether other factors, such as additional substances taken or hepatitis C virus (HCV) infection, are responsible. NPS abusers are at particular risk of HCV infection, and for this reason, it is all the more important to determine what factors actually show a hepatotoxic effect in them. Full article
(This article belongs to the Special Issue Liver Diseases: From Bench to Bedside)
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