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Biomolecules
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Targets and Treatment Approaches for End-Stage Liver Diseases
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Targets and Treatment Approaches for End-Stage Liver Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 26382

Special Issue Editors

Prof. Dr. Natalia Osna

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Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veteran Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-8080, USA
Interests: hepatitis C, B, HIV, and other viral hepatitis; alcohol-associated liver disease; innate immunity; antigen presentation; proteasome; protein posttranslational modifications; animal models for a hepatitis study; long-acting drugs
Special Issues, Collections and Topics in MDPI journals
Dr. Benita McVicker

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veterans Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-1850, USA
Interests: alcohol-associated liver disease; protein trafficking; tumor-associated macrophages; colorectal liver metastasis
Dr. Saraswathi Viswanathan

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veterans Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-1850, USA
Interests: obesity; alcoholic and non-alcoholic liver disease; insulin resistance; metabolism; pancreatic cancer

Special Issue Information

Dear Colleagues, 

This Special Issue is designed to cover multiple targets and treatments of end-stage liver diseases, such as fibrosis, cirrhosis, and liver cancers. We welcome original research and review articles of a broad spectrum, including experimental approaches for targeting pathologically important mechanisms, the outlook of therapeutic development, as well as the results of clinical trials.

Prof. Dr. Natalia Osna
Dr. Benita McVicker
Dr. Saraswathi Viswanathan
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. Biomolecules is an international peer-reviewed open access monthly 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 2700 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.

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Published Papers (7 papers)

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Research

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16 pages, 6002 KiB  
Article
Establishment of a Rat Model of Alcoholic Liver Fibrosis with Simulated Human Drinking Patterns and Low-Dose Chemical Stimulation
by Chien-Yu Lin, Evanthia Omoscharka, Yanli Liu and Kun Cheng
Biomolecules 2023, 13(9), 1293; https://doi.org/10.3390/biom13091293 - 24 Aug 2023
Cited by 1 | Viewed by 1939
Abstract
Although alcohol is a well-known causal factor associated with liver diseases, challenges remain in inducing liver fibrosis in experimental rodent models. These challenges include rodents’ natural aversion to high concentrations of alcohol, rapid alcohol metabolism, the need for a prolonged duration of alcohol [...] Read more.
Although alcohol is a well-known causal factor associated with liver diseases, challenges remain in inducing liver fibrosis in experimental rodent models. These challenges include rodents’ natural aversion to high concentrations of alcohol, rapid alcohol metabolism, the need for a prolonged duration of alcohol administration, and technical difficulties. Therefore, it is crucial to establish an experimental model that can replicate the features of alcoholic liver fibrosis. The objective of this study was to develop a feasible rat model of alcoholic liver fibrosis that emulates human drinking patterns and combines low-dose chemicals within a relatively short time frame. We successfully developed an 8-week rat model of alcoholic liver fibrosis that mimics chronic and heavy drinking patterns. Rats were fed with a control liquid diet, an alcohol liquid diet, or alcohol liquid diet combined with multiple binges via oral gavage. To accelerate the progression of alcoholic liver fibrosis, we introduced low-dose carbon tetrachloride (CCl4) through intraperitoneal injection. This model allows researchers to efficiently evaluate potential therapeutics in preclinical studies of alcoholic liver fibrosis within a reasonable time frame. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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13 pages, 3699 KiB  
Article
Peptide-Based siRNA Nanocomplexes Targeting Hepatic Stellate Cells
by Chien-Yu Lin, Umar-Farouk Mamani, Yuhan Guo, Yanli Liu and Kun Cheng
Biomolecules 2023, 13(3), 448; https://doi.org/10.3390/biom13030448 - 28 Feb 2023
Cited by 6 | Viewed by 2646
Abstract
Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) in the liver due to chronic injuries and inflammation. These injuries activate and transform quiescent hepatic stellate cells (HSCs) into proliferative myofibroblast-like cells, which are the key contributors to the secretin of ECM [...] Read more.
Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) in the liver due to chronic injuries and inflammation. These injuries activate and transform quiescent hepatic stellate cells (HSCs) into proliferative myofibroblast-like cells, which are the key contributors to the secretin of ECM in the fibrotic liver. The insulin-like growth factor 2 receptor (IGF2R) is a multifunctional receptor that is overexpressed on activated HSCs and is a specific molecular marker of activated HSCs in the fibrotic liver. We recently discovered an IGF2R-specific peptide that significantly increases the binding affinity and uptake of a protein-based siRNA nanocomplex to activated HSCs. However, there is a potential concern about the immunogenicity of protein-based siRNA delivery systems. In this study, we used the IGF2R-specific peptide to modify a small peptide-based siRNA nanocomplex for HSC-specific drug delivery. We incorporated a short spacer and glutamate residues into the IGF2R peptides. The siRNA nanocomplex modified with the IGF2R-3GK6E peptide demonstrated higher HSC specificity compared to an unmodified nanocomplex. This peptide-based nanocomplex provides a promising platform to effectively deliver Pcbp2 siRNA to activated HSCs for the treatment of liver fibrosis. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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17 pages, 7475 KiB  
Article
IL-18BP Improves Early Graft Function and Survival in Lewis–Brown Norway Rat Orthotopic Liver Transplantation Model
by Qiang Meng, Weikang Wu, Wenjie Zhang, Juzheng Yuan, Long Yang, Xuan Zhang and Kaishan Tao
Biomolecules 2022, 12(12), 1801; https://doi.org/10.3390/biom12121801 - 1 Dec 2022
Cited by 3 | Viewed by 2288
Abstract
Interleukin-18 (IL-18) can effectively activate natural killer (NK) cells and induce large concentrations of interferon-γ (IFN-γ). In healthy humans, IL-18 binding protein (IL-18BP) can inhibit the binding of IL-18 to IL-18R and counteract the biological action of IL-18 due to its high concentration [...] Read more.
Interleukin-18 (IL-18) can effectively activate natural killer (NK) cells and induce large concentrations of interferon-γ (IFN-γ). In healthy humans, IL-18 binding protein (IL-18BP) can inhibit the binding of IL-18 to IL-18R and counteract the biological action of IL-18 due to its high concentration and high affinity, thus preventing the production of IFN-γ and inhibiting NK-cell activation. Through previous studies and the phenomena observed by our group in pig–non-human primates (NHPs) liver transplantation experiments, we proposed that the imbalance in IL-18/IL-18BP expression upon transplantation encourages the activation, proliferation, and cytotoxic effects of NK cells, ultimately causing acute vascular rejection of the graft. In this research, we used Lewis–Brown Norway rat orthotopic liver transplantation (OLTx) as a model of acute vascular rejection. AAV8-Il18bp viral vectors as gene delivery vehicles were constructed for gene therapy to overexpress IL-18BP and alleviate NK-cell rejection of the graft after transplantation. The results showed that livers overexpressing IL-18BP had reduced damage and could function longer after transplantation, effectively improving the survival time of the recipients. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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Review

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22 pages, 3328 KiB  
Review
Regulation of Fructose Metabolism in Nonalcoholic Fatty Liver Disease
by Mareca Lodge, Rachel Dykes and Arion Kennedy
Biomolecules 2024, 14(7), 845; https://doi.org/10.3390/biom14070845 - 13 Jul 2024
Cited by 2 | Viewed by 3181
Abstract
Elevations in fructose consumption have been reported to contribute significantly to an increased incidence of obesity and metabolic diseases in industrial countries. Mechanistically, a high fructose intake leads to the dysregulation of glucose, triglyceride, and cholesterol metabolism in the liver, and causes elevations [...] Read more.
Elevations in fructose consumption have been reported to contribute significantly to an increased incidence of obesity and metabolic diseases in industrial countries. Mechanistically, a high fructose intake leads to the dysregulation of glucose, triglyceride, and cholesterol metabolism in the liver, and causes elevations in inflammation and drives the progression of nonalcoholic fatty liver disease (NAFLD). A high fructose consumption is considered to be toxic to the body, and there are ongoing measures to develop pharmaceutical therapies targeting fructose metabolism. Although a large amount of work has summarized the effects fructose exposure within the intestine, liver, and kidney, there remains a gap in our knowledge regarding how fructose both indirectly and directly influences immune cell recruitment, activation, and function in metabolic tissues, which are essential to tissue and systemic inflammation. The most recent literature demonstrates that direct fructose exposure regulates oxidative metabolism in macrophages, leading to inflammation. The present review highlights (1) the mechanisms by which fructose metabolism impacts crosstalk between tissues, nonparenchymal cells, microbes, and immune cells; (2) the direct impact of fructose on immune cell metabolism and function; and (3) therapeutic targets of fructose metabolism to treat NAFLD. In addition, the review highlights how fructose disrupts liver tissue homeostasis and identifies new therapeutic targets for treating NAFLD and obesity. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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22 pages, 1526 KiB  
Review
Chronic Hepatitis B Infection: New Approaches towards Cure
by Mojisola Ogunnaike, Srijanee Das, Samiksha S. Raut, Ashrafi Sultana, Mohammad Ullah Nayan, Murali Ganesan, Benson J. Edagwa, Natalia A. Osna and Larisa Y. Poluektova
Biomolecules 2023, 13(8), 1208; https://doi.org/10.3390/biom13081208 - 1 Aug 2023
Cited by 7 | Viewed by 7809
Abstract
Chronic hepatitis B virus (HBV) infection leads to the development of cirrhosis and hepatocellular carcinoma. Lifelong treatment with nucleotides/nucleoside antiviral agents is effective at suppressing HBV replication, however, adherence to daily therapy can be challenging. This review discusses recent advances in the development [...] Read more.
Chronic hepatitis B virus (HBV) infection leads to the development of cirrhosis and hepatocellular carcinoma. Lifelong treatment with nucleotides/nucleoside antiviral agents is effective at suppressing HBV replication, however, adherence to daily therapy can be challenging. This review discusses recent advances in the development of long-acting formulations for HBV treatment and prevention, which could potentially improve adherence. Promising new compounds that target distinct steps of the virus life cycle are summarized. In addition to treatments that suppress viral replication, curative strategies are focused on the elimination of covalently closed circular DNA and the inactivation of the integrated viral DNA from infected hepatocytes. We highlight promising long-acting antivirals and genome editing strategies for the elimination or deactivation of persistent viral DNA products in development. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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13 pages, 1366 KiB  
Review
The SLIT/ROBO Pathway in Liver Fibrosis and Cancer
by Sreenivasulu Basha, Brady Jin-Smith, Chunbao Sun and Liya Pi
Biomolecules 2023, 13(5), 785; https://doi.org/10.3390/biom13050785 - 1 May 2023
Cited by 10 | Viewed by 4372
Abstract
Liver fibrosis is a common outcome of most chronic liver insults/injuries that can develop into an irreversible process of cirrhosis and, eventually, liver cancer. In recent years, there has been significant progress in basic and clinical research on liver cancer, leading to the [...] Read more.
Liver fibrosis is a common outcome of most chronic liver insults/injuries that can develop into an irreversible process of cirrhosis and, eventually, liver cancer. In recent years, there has been significant progress in basic and clinical research on liver cancer, leading to the identification of various signaling pathways involved in tumorigenesis and disease progression. Slit glycoprotein (SLIT)1, SLIT2, and SLIT3 are secreted members of a protein family that accelerate positional interactions between cells and their environment during development. These proteins signal through Roundabout receptor (ROBO) receptors (ROBO1, ROBO2, ROBO3, and ROBO4) to achieve their cellular effects. The SLIT and ROBO signaling pathway acts as a neural targeting factor regulating axon guidance, neuronal migration, and axonal remnants in the nervous system. Recent findings suggest that various tumor cells differ in SLIT/ROBO signaling levels and show varying degrees of expression patterns during tumor angiogenesis, cell invasion, metastasis, and infiltration. Emerging roles of the SLIT and ROBO axon-guidance molecules have been discovered in liver fibrosis and cancer development. Herein, we examined the expression patterns of SLIT and ROBO proteins in normal adult livers and two types of liver cancers: hepatocellular carcinoma and cholangiocarcinoma. This review also summarizes the potential therapeutics of this pathway for anti-fibrosis and anti-cancer drug development. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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13 pages, 1375 KiB  
Review
Effect of Ethanol on Exosome Biogenesis: Possible Mechanisms and Therapeutic Implications
by Vaishnavi Sundar and Viswanathan Saraswathi
Biomolecules 2023, 13(2), 222; https://doi.org/10.3390/biom13020222 - 24 Jan 2023
Cited by 4 | Viewed by 2847
Abstract
Most eukaryotic cells, including hepatocytes, secrete exosomes into the extracellular space, which are vesicles facilitating horizontal cell-to-cell communication of molecular signals and physiological cues. The molecular cues for cellular functions are carried by exosomes via specific mRNAs, microRNAs, and proteins. Exosomes released by [...] Read more.
Most eukaryotic cells, including hepatocytes, secrete exosomes into the extracellular space, which are vesicles facilitating horizontal cell-to-cell communication of molecular signals and physiological cues. The molecular cues for cellular functions are carried by exosomes via specific mRNAs, microRNAs, and proteins. Exosomes released by liver cells are a vital part of biomolecular communication in liver diseases. Importantly, exosomes play a critical role in mediating alcohol-associated liver disease (ALD) and are potential biomarkers for ALD. Moreover, alcohol exposure itself promotes exosome biogenesis and release from the livers of humans and rodent models. However, the mechanisms by which alcohol promotes exosome biogenesis in hepatocytes are still unclear. Of note, alcohol exposure leads to liver injury by modulating various cellular processes, including autophagy, ER stress, oxidative stress, and epigenetics. Evidence suggests that there is a link between each of these processes with exosome biogenesis. The aim of this review article is to discuss the interplay between ethanol exposure and these altered cellular processes in promoting hepatocyte exosome biogenesis and release. Based on the available literature, we summarize and discuss the potential mechanisms by which ethanol induces exosome release from hepatocytes, which in turn leads to the progression of ALD. Full article
(This article belongs to the Special Issue Targets and Treatment Approaches for End-Stage Liver Diseases)
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