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Chronic Liver Disease and Hepatocellular Carcinoma—2nd Edition
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Chronic Liver Disease and Hepatocellular Carcinoma—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 591

Special Issue Editors

Dr. Daniela Gabbia

E-Mail Website
Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, L.go Meneghetti 2, 35131 Padova, Italy
Interests: chronic liver disease; hepatocellular carcinoma; liver metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Sara Carpi

E-Mail Website
Guest Editor
1. Department of Health Sciences, University ‘Magna Græcia’ of Catanzaro, Viale Europa, Località Germaneto, 88100 Catanzaro, Italy
2. NEST, Istituto Nanoscienze-CNR and Scuola Normale Superiore, Piazza San Silvestro 12, 56127 Pisa, Italy
Interests: pharmacology; molecular pharmacology; demyelination; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic liver disease of different aetiologies, such as viral, metabolic-derived, or autoimmune pathologies, represents a major risk factor for the development of hepatocellular carcinoma (HCC). This primary liver malignancy has been the sixth most diagnosed cancer in 2020, and the third leading cause of cancer-related death worldwide. Due to high morbidity and mortality, as well as growing incidence, HCC represents a global health challenge. Since about 80% of patients develop HCC as consequence of chronic liver disease and cirrhosis, many studies are focusing on unravelling the molecular mechanisms responsible for its development and progression in order to find new therapeutic targets and predictive marker of its prognosis that could prevent the progression of chronic disease to cancer. Studies that focus on this topic are welcome in this Special Issue.

This Special Issue aims to provide new insights on novel molecular targets, therapeutic options, and/or biomarkers which could be helpful in preventing the progression of chronic liver disease to HCC and that could potentially be exploited in clinical development. Studies investigating naturally derived materials are also welcome, even though they must report a precise description of the active ingredients of the plant extract.

Dr. Daniela Gabbia
Dr. Sara Carpi
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

  • hepatocellular carcinoma
  • NAFLD/NASH
  • viral hepatitis
  • autoimmune liver disease
  • immunotherapy
  • biomarker

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Published Papers (2 papers)

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Research

16 pages, 3966 KiB  
Article
Gut Microbiota and Its Metabolite Taurine-β-Muricholic Acid Contribute to Antimony- and/or Copper-Induced Liver Inflammation
by Dandan Wu, Qiwen Lin, Senao Hou, Xiaorui Cui, Na Shou, Xuefeng Yuan, Wenqian Xu, Keyi Fu, Qi Wang and Zunji Shi
Int. J. Mol. Sci. 2025, 26(7), 3332; https://doi.org/10.3390/ijms26073332 (registering DOI) - 3 Apr 2025
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Abstract
Antimony and copper can contaminate vegetables and enter the human body through the digestive tract, inducing severe and extensive biotoxicity. However, the role of bile acids (BAs) in the pathogenesis of liver inflammation by antimony or copper has not been elucidated. Our results [...] Read more.
Antimony and copper can contaminate vegetables and enter the human body through the digestive tract, inducing severe and extensive biotoxicity. However, the role of bile acids (BAs) in the pathogenesis of liver inflammation by antimony or copper has not been elucidated. Our results indicated that antimony and/or copper induced liver inflammation, causing the disruption of gut microbiota, with the down-regulation of probiotics and up-regulation of harmful bacteria closely correlated to liver inflammation. Targeted metabolomics of BAs showed that antimony and/or copper significantly up-regulated the levels of taurine-β-muricholic acid (T-β-MCA) in serum and liver, which was due to the reduction of Lactobacillus spp. A farnesoid X receptor (FXR) antagonist, T-β-MCA inhibited the FXR-SHP pathway in liver and FXR-FGF15 pathway in ileum, thereby promoting the transcription of cholesterol 7-alpha hydroxylase (CYP7A1) and increasing total bile acid concentrations, ultimately leading to liver inflammation. These findings provide new insights into the underlying mechanisms of antimony- and/or copper-induced liver inflammation. Full article
(This article belongs to the Special Issue Chronic Liver Disease and Hepatocellular Carcinoma—2nd Edition)
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18 pages, 3443 KiB  
Article
Flutamide Promotes Early Hepatocarcinogenesis Through Mitophagy in High-Fat Diet-Fed Non-Obese Steatotic Rats
by Emika Hara, Kanami Ohshima, Mio Takimoto, Yidan Bai, Mai Hirata, Wen Zeng, Suzuka Uomoto, Mai Todoroki, Mio Kobayashi, Takuma Kozono, Tetsuhito Kigata, Makoto Shibutani and Toshinori Yoshida
Int. J. Mol. Sci. 2025, 26(6), 2709; https://doi.org/10.3390/ijms26062709 - 17 Mar 2025
Viewed by 279
Abstract
Flutamide (FL), a non-steroidal drug used for its antiandrogenic, anticancer, and disrupting endocrine properties, induces mitochondrial toxicity and drug metabolism enzymes and promotes hepatocarcinogenesis. The inhibition of mitophagy, leading to the accumulation of damaged mitochondria, is implicated in the pathogenesis of nonalcoholic fatty [...] Read more.
Flutamide (FL), a non-steroidal drug used for its antiandrogenic, anticancer, and disrupting endocrine properties, induces mitochondrial toxicity and drug metabolism enzymes and promotes hepatocarcinogenesis. The inhibition of mitophagy, leading to the accumulation of damaged mitochondria, is implicated in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the effects of FL in high-fat diet (HFD)-induced non-obese steatosis rats, categorized into four groups: basal diet (BD), BD + FL, HFD, and HFD + FL. The FL exacerbated HFD-induced steatosis and marginally increased preneoplastic lesions. To analyze hepatic preneoplastic lesions, we divided them into clusters based on the expression ratios of the mitophagy regulators LC3 and AMBRA1. The expression rates of LC3 and AMBRA1 in these precancerous lesions were classified into three clusters using k-means clustering. The HFD group exhibited an increased ratio of mitophagy inhibition clusters, as indicated by decreased LC3 and increased AMBRA1 levels in background hepatocytes and preneoplastic lesions. FL counteracted HFD-mediated mitophagy inhibition, as indicated by increased LC3 and decreased AMBRA1 levels in background hepatocytes. Our clustering analysis revealed that FL-induced mitophagy induction relied on Parkin expression. The present study underscores the significance of cluster analysis in understanding the role of mitophagy within small preneoplastic lesions and suggests that FL may potentially exacerbate NAFLD-associated hepatocarcinogenesis by affecting mitophagy. Full article
(This article belongs to the Special Issue Chronic Liver Disease and Hepatocellular Carcinoma—2nd Edition)
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