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Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases
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Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases

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 (15 November 2022) | Viewed by 10874

Special Issue Editor

Dr. Tatsuo Kanda

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University, School of Medicine 30-1, Oyaguchi-Kamicho, Itabashi-Ku, Tokyo 173-8610, Japan
Interests: viral hepatitis; hepatocellular carcinoma; innate immunity; unfolded protein response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Welcome to this Special Issue, “Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases”, of the International Journal of Molecular Sciences. Interferon-free treatment against hepatitis C virus (HCV) is currently available, and its efficacy is higher, with fewer adverse events and a shorter duration, although there are several problems, such as the occurrence of hepatocellular carcinoma (HCC) after a sustained virological response (SVR), the reactivation of hepatitis B virus (HBV) and drug-resistance-associated substitutions (RASs). New cancer immune therapies, such as the blockers of immune checkpoints, also have high efficacies and cause liver injuries. This Special Issue will present the recent findings related to viral hepatitis, other liver diseases and liver-related gastrointestinal diseases. Original research and review articles on all topics in this area are invited for submission. We also have great interest in molecular research, such as resistance-mutations and host responses. It is our greatest pleasure to invite research scientists and clinicians from all relevant fields to submit their articles for this Special Issue. Please accept my special thanks for choosing to publish in the International Journal of Molecular Sciences. We are looking forward to your submissions for this highly important Special Issue.

Dr. Tatsuo Kanda
Guest Editor

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

  • viral hepatitis
  • DAA
  • NASH
  • drug-induced liver injury
  • HCC
  • cirrhosis

Published Papers (6 papers)

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Editorial

Jump to: Research, Review, Other

3 pages, 197 KiB  
Editorial
Molecular Mechanism of Chronic Viral and Non-Viral Liver Diseases
by Tatsuo Kanda
Int. J. Mol. Sci. 2023, 24(7), 6218; https://doi.org/10.3390/ijms24076218 - 25 Mar 2023
Viewed by 963
Abstract
In this Special Issue, “Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases”, invaluable articles have been published [...] Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)

Research

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12 pages, 1326 KiB  
Article
Autoantibodies to PAX5, PTCH1, and GNA11 as Serological Biomarkers in the Detection of Hepatocellular Carcinoma in Hispanic Americans
by Cuipeng Qiu, Yangcheng Ma, Bofei Wang, Xiaojun Zhang, Xiao Wang and Jian-Ying Zhang
Int. J. Mol. Sci. 2023, 24(4), 3721; https://doi.org/10.3390/ijms24043721 - 13 Feb 2023
Cited by 3 | Viewed by 1268
Abstract
Studies have demonstrated that autoantibodies to tumor-associated antigens (TAAs) may be used as efficient biomarkers with low-cost and highly sensitive characteristics. In this study, an enzyme-linked immunosorbent assay (ELISA) was conducted to analyze autoantibodies to paired box protein Pax-5 (PAX5), protein patched homolog [...] Read more.
Studies have demonstrated that autoantibodies to tumor-associated antigens (TAAs) may be used as efficient biomarkers with low-cost and highly sensitive characteristics. In this study, an enzyme-linked immunosorbent assay (ELISA) was conducted to analyze autoantibodies to paired box protein Pax-5 (PAX5), protein patched homolog 1 (PTCH1), and guanine nucleotide-binding protein subunit alpha-11 (GNA11) in sera from Hispanic Americans including hepatocellular carcinoma (HCC) patients, patients with liver cirrhosis (LC), patients with chronic hepatitis (CH), as well as normal controls. Meanwhile, 33 serial sera from eight HCC patients before and after diagnosis were used to explore the potential of these three autoantibodies as early biomarkers. In addition, an independent non-Hispanic cohort was used to evaluate the specificity of these three autoantibodies. In the Hispanic cohort, at the 95.0% specificity for healthy controls, 52.0%, 44.0%, and 44.0% of HCC patients showed significantly elevated levels of autoantibodies to PAX5, PTCH1, and GNA11, respectively. Among patients with LC, the frequencies for autoantibodies to PAX5, PTCH1, and GNA11 were 32.1%, 35.7%, and 25.0%, respectively. The area under the ROC curves (AUCs) of autoantibodies to PAX5, PTCH1, and GNA11 for identifying HCC from healthy controls were 0.908, 0.924, and 0.913, respectively. When these three autoantibodies were combined as a panel, the sensitivity could be improved to 68%. The prevalence of PAX5, PTCH1, and GNA11 autoantibodies has already occurred in 62.5%, 62.5%, or 75.0% of patients before clinical diagnosis, respectively. In the non-Hispanic cohort, autoantibodies to PTCH1 showed no significant difference; however, autoantibodies to PAX5, PTCH1, and GNA11 showed potential value as biomarkers for early detection of HCC in the Hispanic population and they may monitor the transition of patients with high-risk (LC, CH) to HCC. Using a panel of the three anti-TAA autoantibodies may enhance the detection of HCC. Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)
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13 pages, 798 KiB  
Article
MTARC1 and HSD17B13 Variants Have Protective Effects on Non-Alcoholic Fatty Liver Disease in Patients Undergoing Bariatric Surgery
by Piotr Kalinowski, Wiktor Smyk, Małgorzata Nowosad, Rafał Paluszkiewicz, Łukasz Michałowski, Bogna Ziarkiewicz-Wróblewska, Susanne N. Weber, Piotr Milkiewicz, Frank Lammert, Krzysztof Zieniewicz and Marcin Krawczyk
Int. J. Mol. Sci. 2022, 23(24), 15825; https://doi.org/10.3390/ijms232415825 - 13 Dec 2022
Cited by 5 | Viewed by 1929
Abstract
The severity of hepatic steatosis is modulated by genetic variants, such as patatin-like phospholipase domain containing 3 (PNPLA3) rs738409, transmembrane 6 superfamily member 2 (TM6SF2) rs58542926, and membrane-bound O-acyltransferase domain containing 7 (MBOAT7) rs641738. Recently, mitochondrial amidoxime [...] Read more.
The severity of hepatic steatosis is modulated by genetic variants, such as patatin-like phospholipase domain containing 3 (PNPLA3) rs738409, transmembrane 6 superfamily member 2 (TM6SF2) rs58542926, and membrane-bound O-acyltransferase domain containing 7 (MBOAT7) rs641738. Recently, mitochondrial amidoxime reducing component 1 (MTARC1) rs2642438 and hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) rs72613567 polymorphisms were shown to have protective effects on liver diseases. Here, we evaluate these variants in patients undergoing bariatric surgery. A total of 165 patients who underwent laparoscopic sleeve gastrectomy and intraoperative liver biopsies and 314 controls were prospectively recruited. Genotyping was performed using TaqMan assays. Overall, 70.3% of operated patients presented with hepatic steatosis. NASH (non-alcoholic steatohepatitis) was detected in 28.5% of patients; none had cirrhosis. The increment of liver fibrosis stage was associated with decreasing frequency of the MTARC1 minor allele (p = 0.03). In multivariate analysis MTARC1 was an independent protective factor against fibrosis ≥ 1b (OR = 0.52, p = 0.03) and ≥ 1c (OR = 0.51, p = 0.04). The PNPLA3 risk allele was associated with increased hepatic steatosis, fibrosis, and NASH (OR = 2.22, p = 0.04). The HSD17B13 polymorphism was protective against liver injury as reflected by lower AST (p = 0.04) and ALT (p = 0.03) activities. The TM6SF2 polymorphism was associated with increased ALT (p = 0.04). In conclusion, hepatic steatosis is common among patients scheduled for bariatric surgery, but the MTARC1 and HSD17B13 polymorphisms lower liver injury in these individuals. Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)
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11 pages, 1773 KiB  
Article
Antiviral Compounds Screening Targeting HBx Protein of the Hepatitis B Virus
by Yaojia Ma, Shingo Nakamoto, Junjie Ao, Na Qiang, Tadayoshi Kogure, Keita Ogawa, Miyuki Nakagawa, Kisako Fujiwara, Terunao Iwanaga, Ryuta Kojima, Hiroaki Kanzaki, Keisuke Koroki, Kazufumi Kobayashi, Naoya Kanogawa, Soichiro Kiyono, Masato Nakamura, Takayuki Kondo, Ryo Nakagawa, Sadahisa Ogasawara, Ryosuke Muroyama, Tetsuhiro Chiba, Jun Kato and Naoya Katoadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2022, 23(19), 12015; https://doi.org/10.3390/ijms231912015 - 10 Oct 2022
Cited by 7 | Viewed by 1997
Abstract
A functional cure of hepatitis B virus (HBV) infection or HB antigen loss is rarely achieved by nucleos(t)ide analogs which target viral polymerase. HBx protein is a regulatory protein associated with HBV replication. We thought to identify antiviral compounds targeting HBx protein by [...] Read more.
A functional cure of hepatitis B virus (HBV) infection or HB antigen loss is rarely achieved by nucleos(t)ide analogs which target viral polymerase. HBx protein is a regulatory protein associated with HBV replication. We thought to identify antiviral compounds targeting HBx protein by analyzing HBx binding activity. Recombinant GST-tagged HBx protein was applied on an FDA-approved drug library chip including 1018 compounds to determine binding affinity by surface plasmon resonance imaging (SPRi) using a PlexArray HT system. GST protein alone was used for control experiments. Candidate compounds were tested for anti-HBV activity as well as cell viability using HepG2.2.15.7 cells and HBV-infected human hepatocytes. Of the 1018 compounds screened, 24 compounds showed binding to HBx protein. Of the top 6 compounds with high affinity to HBx protein, tranilast was found to inhibit HBV replication without affecting cell viability using HepG2.2.15.7 cells. Tranilast also inhibited HBV infection using cultured human hepatocytes. Tranilast reduced HB antigen level dose-dependently. Overall, theSPRi screening assay identified novel drug candidates targeting HBx protein. Tranilast and its related compounds warrant further investigation for the treatment of HBV infection. Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)
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Review

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12 pages, 1049 KiB  
Review
Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
by Reina Sasaki-Tanaka, Ranjit Ray, Mitsuhiko Moriyama, Ratna B. Ray and Tatsuo Kanda
Int. J. Mol. Sci. 2022, 23(17), 9679; https://doi.org/10.3390/ijms23179679 - 26 Aug 2022
Cited by 10 | Viewed by 2665
Abstract
Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. [...] Read more.
Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease. Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)
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Other

5 pages, 1323 KiB  
Case Report
Genotype–Phenotype Association in ABCC2 Exon 18 Missense Mutation Leading to Dubin–Johnson Syndrome: A Case Report
by Ji-Hoon Kim, Min-Woo Kang, Sangmi Kim, Ji Won Han, Jeong Won Jang, Jong Young Choi, Seung Kew Yoon and Pil Soo Sung
Int. J. Mol. Sci. 2022, 23(24), 16168; https://doi.org/10.3390/ijms232416168 - 18 Dec 2022
Cited by 1 | Viewed by 1579
Abstract
We report a case of a patient with Dubin–Johnson syndrome confirmed by a genetic study. A 50-year-old woman who had symptoms of intermittent right upper quadrant abdominal pain was diagnosed with calculous cholecystitis at another institute and was presented to our hospital for [...] Read more.
We report a case of a patient with Dubin–Johnson syndrome confirmed by a genetic study. A 50-year-old woman who had symptoms of intermittent right upper quadrant abdominal pain was diagnosed with calculous cholecystitis at another institute and was presented to our hospital for a cholecystectomy. She had no history of liver disease, and her physical examination was normal. Abdominal computed tomography showed a gallbladder stone with chronic cholecystitis. During a laparoscopic cholecystectomy for cholecystitis, a smooth, black-colored liver was noted, and a liver biopsy was performed. The biopsy specimen showed coarse, dark brown granules in centrilobular hepatocytes via hematoxylin and eosin staining. We performed a genetic study using the blood samples of the patient. In the adenosine triphosphate-binding cassette subfamily C member 2 (ABCC2) mutation study, a missense mutation in exon 18 was noted. Based on the black-colored liver without nodularity, conjugated hyperbilirubinemia, the liver biopsy results of the coarse pigment in centrilobular hepatocytes, and the ABCC2 mutation, Dubin–Johnson syndrome was diagnosed. The patient was managed with conservative care using hepatotonics. One month after follow-up, total bilirubin and direct bilirubin remained in a similar range. Another follow-up was planned a month later, and the patient maintained her use of hepatotonics. Full article
(This article belongs to the Special Issue Molecular Mechanism of Chronic Viral and Non-viral Liver Diseases)
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