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Molecular Insights in Hepatic Disease and Hepatocellular Carcinoma
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Molecular Insights in Hepatic Disease and Hepatocellular Carcinoma

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: 20 August 2025 | Viewed by 848

Special Issue Editors

Dr. Soon Kyu Lee

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea
Interests: hepatic diseases and hepatocellular carcinoma
Dr. Jong-Young Choi

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea
Interests: hepatic diseases and hepatocellular carcinoma

Special Issue Information

Dear Colleagues,

The field of hepatology has witnessed remarkable research and revolutionary developments in recent years. Particularly in the treatment of advanced hepatocellular carcinoma (HCC), the widespread use of immune checkpoint inhibitors presents the potential to extend treatment efficacy to early and intermediate stages of HCC. In the field of viral hepatitis, significant progress has been marked by the use of high-potency nucleos(t)ide analogues. Additionally, several clinical trials are implementing new drug combinations aimed at achieving an HBV cure. Additionally, in the realm of fatty liver disease, a new term—metabolic dysfunction-associated steatotic liver disease—has been introduced, with numerous promising drugs currently undergoing clinical trials.

In alignment with these revolutionary strides, this Special Issue aims to provide an overview of molecular insights in hepatic diseases and hepatocellular carcinoma. It will encompass various basic and translational research related to a spectrum of hepatic disorders. We therefore invite you to submit research papers to this Special Issue.

Potential topics include, but are not limited to: 

  • Hepatology;
  • Viral hepatitis;
  • Metabolic dysfunction-associated steatotic liver disease;
  • Alcohol-associated liver disease;
  • Liver cirrhosis;
  • Hepatocellular carcinoma;
  • Liver transplantation;
  • Mechanisms of action;
  • Molecular research;
  • Antivirals;
  • Molecular targeting therapy;
  • Immune checkpoint inhibitor.

Dr. Soon Kyu Lee
Dr. Jong-Young Choi
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
  • liver cirrhosis
  • hepatocellular carcinoma
  • liver transplantation

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Published Papers (1 paper)

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Research

20 pages, 4306 KiB  
Article
Caveolin-1 Deficiency in Macrophages Alleviates Carbon Tetra-Chloride-Induced Acute Liver Injury in Mice
by Ruirui Li, Yixue Shu, Yulin Yan, Junyi Zhu, Zilu Cheng, Jie Zhang, Liming Zhu, Yanhua Qiao and Quan Sun
Int. J. Mol. Sci. 2025, 26(10), 4903; https://doi.org/10.3390/ijms26104903 - 20 May 2025
Viewed by 360
Abstract
Bone marrow-derived macrophages (BMMs) exhibit dynamic behavior and functional capabilities in response to specific microenvironmental stimuli. Recent investigations have proved that BMMs play crucial roles in promoting necrotic lesion resolution. Despite substantial advancements in understanding their activation and interaction with injured livers, researchers [...] Read more.
Bone marrow-derived macrophages (BMMs) exhibit dynamic behavior and functional capabilities in response to specific microenvironmental stimuli. Recent investigations have proved that BMMs play crucial roles in promoting necrotic lesion resolution. Despite substantial advancements in understanding their activation and interaction with injured livers, researchers face challenges to develop effective treatments based on manipulating BMMs function. Caveolin-1 (Cav-1) is the major structural protein on the plasma membrane. We previously reported that Cav-1 knockout (KO) mice exhibited less functional damage and necrosis in carbon tetrachloride (CCl4)-induced liver injury. We hypothesize that the activation and recruitment of BMMs are involved in the resolution of necrotic lesions in Cav-1 KO mice. Wild-type (WT) and Cav-1 KO mice were injected with CCl4 (10% v/v) to induce acute liver injury model. Blood samples and hepatic tissues were harvested for serum alanine transaminase (ALT) activity assessment, histopathological examination through hematoxylin–eosin (H&E) staining, and BMMs subpopulation analysis via flow cytometry. Then, primary BMMs were isolated and cultured to investigate the effect of Cav-1 on BMMs polarization, migration, and activation of STAT3 signal pathway. Validation of hepatic macrophage depletion was induced by administrating clodronate liposomes (CLs), and BMMs reconstitution was evaluated by EGFP labelled BMMs. Following this, hepatic macrophages were depleted by CLs, BMMs were isolated from Cav-1 KO, and WT mice were cultured and administrated to evaluate the protective role of Cav-1-deleted BMMs on the resolution of hepatocellular necrosis and apoptosis in acute liver injury. The BMMs ratio significantly increased from 2.12% (1D), 4.38% (1W), and 5.38% (2W) in oil control mice to 7.17%, 14.90%, and 19.30% in CCl4-treated mice (p < 0.01 or p < 0.001). Concurrently, Cav-1 positive BMMs exhibited a marked elevation from 6.41% at 1D to 24.90% by 2W (p = 0.0228). Cav-1 KO exerted protective effects by reducing serum ALT by 26% (p = 0.0265) and necrotic areas by 28% (p = 0.0220) and enhancing BMMs infiltration by 60% (p = 0.0059). In vitro, Cav-1 KO BMMs showed a decrease in CD206 fluorescence intensity (p < 0.001), a time-dependent upregulation of arginase-1 mRNA (p < 0.05 or p < 0.01), a 1.22-fold increase in phosphorylated STAT3 (p = 0.0036), and impaired wound healing from 12 to 24 h (p < 0.001). The macrophage-depleting action in livers by CL injection persists for a minimum of 48 h. Administrated EGFP+ BMMs emerged as the predominant population following CL injection for a duration of 48 h. Following clodronate liposome-mediated hepatic macrophage depletion, the adoptive transfer of Cav-1 KO BMMs demonstrated therapeutic efficacy in CCl4-induced acute liver injury. In CCl4-induced acute liver injury, the adoptive transfer of Cav-1 KO BMMs reduced necrosis by 12.8% (p = 0.0105), apoptosis by 25.2% (p = 0.0127), doubled macrophages infiltration (p = 0.0269), and suppressed CXCL9/10 mRNA expression (p = 0.0044 or p = 0.0385). BMMs play a key role in the resolution of liver necrotic lesions in CCl4-induced acute liver injury. Cav-1 depletion attenuates hepatocellular necrosis and apoptosis by accelerating BMMs recruitment and M2 polarization. Cav-1 in macrophages may represent a potential therapeutic target for acute liver injury. Full article
(This article belongs to the Special Issue Molecular Insights in Hepatic Disease and Hepatocellular Carcinoma)
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