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Molecular Advances and Insights into Liver Diseases: Second Edition

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 March 2027 | Viewed by 2655

Editor

Special Issue Information

Dear Colleagues,

The increasing incidence rate of various liver diseases is induced by numerous factors, which primarily include improper dietary habits, excessive alcohol consumption, components of the metabolic syndrome such as obesity, or risky behaviors that might result in hepatitis. Although the abovementioned factors are commonly known to be associated with liver dysfunctions, current studies are mostly focused on the molecular mechanisms of liver diseases. Liver diseases might occur due to alcohol consumption, viral infection, or medicine. Further, the occurrence of various hepatic dysfunctions can be a result of genetic (Wilson’s disease, hemochromatosis) or autoimmune (cirrhosis, hepatitis) disorders. The abovementioned conditions could be better understood only by focusing on the pathomechanisms occurring on the molecular level that ultimately induce changes leading to these diseases. A better understanding of such processes will result in improvements in both diagnosis and treatment strategies for the chosen liver diseases.

The major objective of this Special Issue is to provide a space for discussion to clinicians and researchers whose studies are focused on the molecular aspects of the chosen liver diseases. This Special Issue aims to also provide a space for the results of novel studies that were performed to improve the diagnosis of liver diseases and, at the same time, provide novel therapeutic options for patients and expand the knowledge on liver disease pathophysiology. Therefore, we are elated to invite you to submit various types of papers including original papers and narrative and systematic reviews to this Special Issue.

Dr. Jacek Baj
Guest Editor

Manuscript Submission Information

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Keywords

  • liver
  • hepatocellular carcinoma
  • cancer
  • hepatitis cirrhosis
  • encephalopathy
  • non-alcoholic fatty liver disease
  • autoimmune diseases
  • Wilson’s disease
  • fatty liver disease

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Published Papers (2 papers)

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Research

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21 pages, 3108 KB  
Article
MicroRNA-34a Promotes Hepatic Lipid Accumulation Through RXRα Suppression and Is Reversed by 9-cis-Retinoic Acid in Steatotic Hepatocytes
by Jai-Sing Yang, Hong-Yi Chiu, Syun-Rong Jhan, Yao-An Liu, Chao-Jung Chen and Shih-Chang Tsai
Int. J. Mol. Sci. 2026, 27(15), 6609; https://doi.org/10.3390/ijms27156609 - 24 Jul 2026
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Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide and is characterized by excessive hepatic lipid accumulation and metabolic dysfunction. Although microRNA-34a (miR-34a) has been implicated in hepatic lipid metabolism, the molecular mechanisms underlying its contribution to MASLD [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide and is characterized by excessive hepatic lipid accumulation and metabolic dysfunction. Although microRNA-34a (miR-34a) has been implicated in hepatic lipid metabolism, the molecular mechanisms underlying its contribution to MASLD remain incompletely understood. Here, we investigated the role of miR-34a in FFA-induced hepatic steatosis using HepG2 cells and explored RXR-associated signaling as a potential therapeutic strategy. RT-qPCR quantified miR-34a expression; direct target interactions were validated using dual-luciferase reporter assays; proteomic alterations were characterized by iTRAQ-based proteomics followed by Ingenuity Pathway Analysis (IPA); and transcriptomic responses to 9-cis-retinoic acid (9-cis-RA) were analyzed by RNA sequencing. FFA treatment significantly increased miR-34a expression, and dual-luciferase assays confirmed that miR-34a directly targets the 3′-UTRs of RXRα, PPARα, and SIRT1. Integrated proteomic and transcriptomic analyses consistently identified LXR/RXR signaling as one of the principal pathways associated with miR-34a dysregulation and 9-cis-RA treatment. Pharmacological activation of RXR-associated signaling with the pan-RXR agonist 9-cis-RA attenuated intracellular lipid accumulation and reduced the expression of key regulators of lipogenesis and fatty acid uptake, including FASN, SCD1, FABP4, and CD36. Collectively, these findings support the miR-34a–RXRα axis as one regulatory component within a broader nuclear receptor network associated with hepatic lipid homeostasis and support further investigation of RXR-associated signaling as a potential therapeutic strategy for MASLD. Nevertheless, confirmation of receptor-specific mechanisms and validation in more physiologically relevant experimental models will be required. Full article
(This article belongs to the Special Issue Molecular Advances and Insights into Liver Diseases: Second Edition)
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Review

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50 pages, 3206 KB  
Review
Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms
by Miłosz Badach, Jakub Banaszek, Kinga Barańska, Jakub Kleinrok, Michał Flieger, Jolanta Flieger, Grzegorz Teresiński, Alicja Forma, Ryszard Sitarz and Jacek Baj
Int. J. Mol. Sci. 2026, 27(12), 5187; https://doi.org/10.3390/ijms27125187 - 8 Jun 2026
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Abstract
Micro- and nanoplastics (MNPs) are emerging environmental contaminants of increasing relevance to human health. Growing evidence suggests that, following ingestion, inhalation, or, less convincingly, dermal exposure, MNPs may cross biological barriers, enter lymphatic and vascular compartments, and reach the liver. Owing to portal [...] Read more.
Micro- and nanoplastics (MNPs) are emerging environmental contaminants of increasing relevance to human health. Growing evidence suggests that, following ingestion, inhalation, or, less convincingly, dermal exposure, MNPs may cross biological barriers, enter lymphatic and vascular compartments, and reach the liver. Owing to portal blood flow, sinusoidal architecture and Kupffer cell activity, the liver appears to be one of the principal sites of early particle sequestration. Human biomonitoring, ex vivo and postmortem studies have detected MNPs in blood and multiple organs, including the liver, although the currently available evidence remains limited and methodologically heterogeneous. Their identification relies on multistep analytical procedures that integrate sample pretreatment with FTIR, Raman spectroscopy, LD-IR, Py-GC-MS and supplementary imaging methods. However, each of these techniques presents significant limitations, particularly in the analysis of nanoplastics. Experimental studies indicate that MNPs may induce hepatic injury through oxidative stress, mitochondrial impairment, endoplasmic reticulum stress, inflammation, DNA damage, dysregulated lipid metabolism and disruption of the gut–liver axis, consequently contributing to steatosis, cholestatic anomalies and fibrosis. Consequently, MNPs should be considered potential contributors to liver pathology, although more comprehensive human data are still required. Full article
(This article belongs to the Special Issue Molecular Advances and Insights into Liver Diseases: Second Edition)
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