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Molecular Mechanisms Driving Liver Disease: From Cellular Stress to Therapeutic Targets

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: 30 September 2026 | Viewed by 2512

Special Issue Editor

Dr. Konstantinos Arvanitakis

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, First Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, St. Kiriakidi 1, 54636 Thessaloniki, Greece
Interests: hepatology; inflammatory bowel disease; gastroenterology; MASLD; hepatocellular carcinoma

Special Issue Information

Dear Colleagues,

Liver diseases represent a growing global health burden, ranging from metabolic dysfunction-associated steatotic liver disease (MASLD) and alcoholic liver disease to fibrosis, cirrhosis, and hepatocellular carcinoma. Despite significant advances, our understanding of the molecular mechanisms that underlie these conditions remains incomplete. Recent discoveries in hepatocellular stress responses, immune interactions, lipid metabolism, and gene regulation are redefining our view of liver disease pathogenesis and opening new therapeutic avenues.

We are pleased to invite you to contribute to this Special Issue, which focuses on unraveling the molecular and cellular basis of liver diseases. By highlighting critical pathways and molecular interactions, we aim to build a platform for knowledge exchange between basic researchers and clinical scientists, fostering translational progress.

This Special Issue aims to bring together high-quality research papers and review articles addressing the molecular underpinnings of liver diseases. The scope aligns closely with the journal’s mission to support research that advances our understanding of disease mechanisms and therapeutic development. Contributions will offer mechanistic insights into liver pathology and suggest new strategies for diagnosis, prevention, and treatment.

Research areas may include (but are not limited to) the following:

  • Endoplasmic reticulum (ER) stress and the unfolded protein response;
  • Mitochondrial dysfunction and metabolic reprogramming;
  • Activation of hepatic stellate cells and fibrogenic signaling;
  • Crosstalk between hepatocytes and immune cells;
  • Non-coding RNAs in liver disease (miRNAs, lncRNAs, circRNAs);
  • Epigenetic and transcriptomic alterations in liver fibrosis and cancer;
  • Molecular drivers of MASLD and MASH progression;
  • Gut–liver axis and the influence of microbial metabolites;
  • Molecular pathways of Hepatocellular Carcinoma development and progression;
  • Single-cell omics and spatial transcriptomics in liver pathology;
  • Target discovery and drug development for liver diseases.

We look forward to receiving your contributions.

Dr. Konstantinos Arvanitakis
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 250 words) can be sent to the Editorial Office for assessment.

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

  • liver disease
  • molecular mechanisms
  • hepatocellular stress
  • fibrosis
  • non-coding RNAs
  • metabolism
  • MASLD
  • liver fibrosis
  • hepatocellular carcinoma
  • therapeutics

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Published Papers (2 papers)

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Research

21 pages, 3220 KB  
Article
Immune and Endothelial-Related Extracellular Vesicles Are Associated with Corticosteroid Response and Mortality in Alcohol-Associated Hepatitis
by Albert Guinart-Cuadra, Anna Brujats, Justyna Szafranska, Rubén Guerrero, Fernándo Dinamarca, Elisabet Cantó, Maria Poca, Eva Román, Elisabet Sánchez-Ardid, Javier Fajardo, Montserrat Camps, Maria Mulet, German Soriano, Àngels Escorsell, Juan M. Falcon-Perez, Esperanza Gonzalez, Andreu Ferrero-Gregori, Cristina Gely, Jorge Villalba, Ramón Bataller, Josepmaria Argemi, Rubén Osuna-Gómez, Silvia Vidal and Edilmar Alvarado-Tapiasadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2026, 27(3), 1258; https://doi.org/10.3390/ijms27031258 - 27 Jan 2026
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Abstract
Alcohol-associated hepatitis (AH) is the most severe clinical manifestation of alcohol-associated liver disease. Corticosteroids are the only disease-specific therapy shown to improve short-term survival. Currently, no non-invasive markers are available to predict patient response to corticosteroids or long-term survival in AH. This study [...] Read more.
Alcohol-associated hepatitis (AH) is the most severe clinical manifestation of alcohol-associated liver disease. Corticosteroids are the only disease-specific therapy shown to improve short-term survival. Currently, no non-invasive markers are available to predict patient response to corticosteroids or long-term survival in AH. This study investigates whether surface antigens on plasma extracellular vesicles (EVs), key mediators of intercellular communication, can reflect the underlying immune dysregulation in AH and serve as prognostic markers. Patients with AH were prospectively enrolled between 2020 and 2024. Blood samples were collected before corticosteroid initiation during the first 24 h of hospitalization. EVs were characterized using nanoparticle tracking analysis, cryo-electron microscopy, and flow cytometry. Interleukin-6 (IL-6), soluble (s)CD62p, Circulating Vascular Cell Adhesion Molecule-1 (sVCAM), tumor necrosis factor receptor superfamily member 1 (TNRFS1a), and Intercellular Adhesion Molecule 1 (ICAM-1) were quantified by ELISA. Key outcome variables included response to corticosteroids and mortality. A total of 46 patients with AH and 28 healthy donors (HD) were included. EV concentration was significantly higher in AH patients than in HD (9.3 × 1011 [IQR 4–24] versus 2.4 × 1011 [IQR 2–4], p = 0.03). Specific EV antigens were associated with key clinical outcomes: CD20 and CD2 levels differed between patients with or without infections (bacterial, viral, and fungal) developed during hospitalization; CD40 and CD146 were elevated in patients who developed acute kidney injury. EVs enriched in monocyte (CD14) and T-reg (CD25) markers were associated with plasma IL-6 levels, while endothelial markers CD105 and CD146 correlated with sVCAM and sCD62p. EVs enriched in platelet (CD49e) and endothelial (CD31) markers were associated with corticosteroid response, whereas EVs enriched with endothelial (CD105 and CD146) and B lymphocyte (CD19) markers were associated with mortality. Overall, EVs enriched in endothelial and monocyte markers may represent a candidate non-invasive tool for predicting corticosteroid response and mortality in AH, aiding risk stratification and early identification of non-responders for timely transplant evaluation. Full article
(This article belongs to the Special Issue Molecular Mechanisms Driving Liver Disease: From Cellular Stress to Therapeutic Targets)
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16 pages, 2693 KB  
Article
Vitamin E Modulates Hepatic Extracellular Adenosine Signaling to Attenuate Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
by Mengting Shan, Magdeline E. Carrasco Apolinario, Tomoko Tokumaru, Kenshiro Shikano, Phurpa Phurpa, Ami Kato, Hitoshi Teranishi, Shinichiro Kume, Nobuyuki Shimizu, Tatsuki Kurokawa, Takatoshi Hikida, Toshikatsu Hanada, Yulong Li and Reiko Hanada
Int. J. Mol. Sci. 2026, 27(2), 614; https://doi.org/10.3390/ijms27020614 - 7 Jan 2026
Viewed by 284
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) involves early disturbances such as excessive lipid accumulation, sterile inflammation, and hepatocellular stress. The results of recent studies have highlighted extracellular ATP and its metabolite adenosine (Ado) as damage-associated molecular patterns (DAMPs) that drive inflammation, endoplasmic reticulum [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) involves early disturbances such as excessive lipid accumulation, sterile inflammation, and hepatocellular stress. The results of recent studies have highlighted extracellular ATP and its metabolite adenosine (Ado) as damage-associated molecular patterns (DAMPs) that drive inflammation, endoplasmic reticulum (ER) stress, and steatosis, contributing to MASLD progression. Although vitamin E is clinically used for its antioxidant and anti-inflammatory properties, it remains unclear whether its therapeutic effects involve modulation of DAMP-associated signaling. To address this gap, we used transgenic zebrafish expressing a liver-specific G-protein-coupled receptor activation-based adenosine sensor (GRABAdo). We found that a high-cholesterol diet markedly increased hepatic extracellular Ado levels, combined with inflammatory and ER stress-associated gene expression. Vitamin E significantly reduced extracellular Ado levels and hepatic lipid accumulation. Based on RNA sequencing results, vitamin E restored the expression of genes encoding calcium-handling proteins, including atp2a1 and atp1b1b. These genes encode components of the sarco/ER Ca2+-ATPase (SERCA) machinery, which is essential for maintaining ER Ca2+ homeostasis and preventing stress-induced hepatic injury. CDN1163-mediated SERCA activation phenocopied the protective effect of vitamin E, supporting a Ca2+-dependent mechanism. Together, these findings highlight extracellular Ado signaling and impaired SERCA-mediated Ca2+ regulation as early drivers of MASLD and demonstrate that vitamin E ameliorates steatosis by targeting both pathways. Full article
(This article belongs to the Special Issue Molecular Mechanisms Driving Liver Disease: From Cellular Stress to Therapeutic Targets)
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