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Biomedicines
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New Challenges in Liver Diseases: From Molecular Pathogenesis to Therapeutic...
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New Challenges in Liver Diseases: From Molecular Pathogenesis to Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 January 2027 | Viewed by 7234

Editor

Prof. Dr. Yefu Wang

E-Mail Website
Guest Editor
The State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, China
Interests: liver fibrosis; cirrhosis; non-alcoholic fatty liver disease (NAFLD); hepatitis B virus (HBV) pathogenesis; acute-on-chronic liver failure (ACLF); immune regulation; therapeutic strategies for chronic liver diseases.

Special Issue Information

Dear Colleagues,

Liver diseases represent a global health crisis, encompassing a broad spectrum of disorders, from viral hepatitis and metabolic dysfunction-associated steatotic liver disease (MASLD) to hepatocellular carcinoma (HCC). Despite advances in diagnostics and therapeutics, challenges persist in understanding molecular mechanisms, achieving functional cures for chronic infections (e.g., HBV), developing clinical treatments for acute-on-chronic liver failure (ACLF), and addressing the rising burden of non-alcoholic steatohepatitis (NASH).

This Special Issue will showcase cutting-edge research on the following topics:

  1. ​Molecular Pathogenesis: Host–virus interactions, epigenetic regulation, metabolic dysregulation, and immune dysfunctions in liver diseases;
  2. ​Therapeutic Innovations: Novel targets (e.g., cccDNA, RNA interference), combination therapies, and precision medicine approaches;
  3. Translational Advances: Non-invasive biomarkers, regenerative medicine, and gut–liver axis modulation;
  4. Global Health Priorities: Elimination strategies for viral hepatitis;

By bridging basic science, clinical research, and innovation, this Special Issue will accelerate the progress toward curing liver diseases and improving patient outcomes worldwide.

Prof. Dr. Yefu Wang
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines 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 2600 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.

Keywords

  • liver fibrosis
  • NAFLD/NASH
  • ACLF
  • HBV cure
  • immunotherapy
  • precision medicine
  • metabolic liver diseases
  • gut–liver axis
  • regenerative medicine
  • biomarkers

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Published Papers (3 papers)

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Review

33 pages, 1000 KB  
Review
HCV-Induced Hepatocarcinogenesis: Molecular Mechanisms, Persistent Cancer Risk, and Future Perspectives
by Snežana Jovanović-Ćupić, Milena Krajnović, Lidija Todorović, Ana Božović and Daniel Galun
Biomedicines 2026, 14(6), 1295; https://doi.org/10.3390/biomedicines14061295 - 7 Jun 2026
Viewed by 456
Abstract
Chronic infection with the hepatitis C virus (HCV) is the most significant risk factor for the development of hepatocellular carcinoma (HCC). It has been shown that the progression of HCV-related liver disease is mediated by both viral and host-specific factors. The HCV replication [...] Read more.
Chronic infection with the hepatitis C virus (HCV) is the most significant risk factor for the development of hepatocellular carcinoma (HCC). It has been shown that the progression of HCV-related liver disease is mediated by both viral and host-specific factors. The HCV replication cycle is a host-dependent process that relies on intracellular signalling pathways within target cells. Thus, intracellular signal transduction plays a pivotal role in the modification of interactions between the host and HCV. These pathways are key regulators of liver diseases, including cirrhosis and HCC. In addition, HCV induces epigenetic modifications in the host genome that inhibit the expression of various tumour-suppressor genes. Some of these changes persist even after successful antiviral treatment and represent a continued risk for HCC development. Despite significant progress in the management of chronic HCV infection, this challenge remains unresolved. In this narrative review, we summarise the mechanisms of HCV-induced disease progression, focusing on the host immune response, the regulatory roles of viral and cellular proteins, and viral survival strategies during chronic infection. We also discuss HCV-induced epigenetic alterations that contribute to hepatocarcinogenesis both during infection and after viral clearance. These insights are important for identifying novel, reliable molecular biomarkers for patient surveillance and for designing new therapeutic approaches. Full article
(This article belongs to the Special Issue New Challenges in Liver Diseases: From Molecular Pathogenesis to Therapeutic Approaches)
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Graphical abstract

19 pages, 1388 KB  
Review
Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation—A Narrative Review
by Héctor Fuentes-Barría, Raúl Aguilera-Eguía, Cherie Flores-Fernández, Lissé Angarita-Davila and Miguel Alarcón-Rivera
Biomedicines 2026, 14(3), 577; https://doi.org/10.3390/biomedicines14030577 - 4 Mar 2026
Viewed by 1382
Abstract
Physical exercise is a potent non-pharmacological strategy for the prevention and management of Metabolic dysfunction—associated steatotic liver disease (MASLD), a multifactorial disorder characterized by hepatic lipid accumulation, insulin resistance, oxidative stress, and chronic inflammation. Emerging evidence demonstrates that the benefits of exercise extend [...] Read more.
Physical exercise is a potent non-pharmacological strategy for the prevention and management of Metabolic dysfunction—associated steatotic liver disease (MASLD), a multifactorial disorder characterized by hepatic lipid accumulation, insulin resistance, oxidative stress, and chronic inflammation. Emerging evidence demonstrates that the benefits of exercise extend beyond caloric expenditure and are largely mediated by coordinated molecular and cellular adaptations within the liver and peripheral tissues. This review synthesizes current knowledge on the mechanisms through which exercise modulates MASLD pathophysiology, emphasizing intracellular signaling pathways, mitochondrial remodeling, antioxidant defenses, and myokine-driven muscle–liver crosstalk. Exercise induces acute and chronic activation of pathways such as AMPK, PGC-1α, Nrf2, and Akt, resulting in enhanced mitochondrial biogenesis, improved fatty acid oxidation, restored insulin signaling, and reduced inflammatory and oxidative stress. Repeated skeletal muscle contraction stimulates the release of myokines—including irisin, IL-6, and FGF21—that act through endocrine and paracrine routes to regulate hepatic lipid metabolism, promote systemic metabolic flexibility, and attenuate disease progression. Epigenetic modifications and exercise-responsive microRNAs further contribute to long-term hepatic metabolic reprogramming. Collectively, these molecular adaptations position exercise as a systemic, disease-modifying stimulus capable of restoring hepatic homeostasis, slowing the transition from steatosis to NASH and fibrosis, and improving long-term metabolic health. Understanding these mechanisms provides a foundation for developing targeted, personalized exercise-based interventions in the clinical management of MASLD. Full article
(This article belongs to the Special Issue New Challenges in Liver Diseases: From Molecular Pathogenesis to Therapeutic Approaches)
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13 pages, 347 KB  
Review
Second-Line Therapies in Primary Biliary Cholangitis: A Comparative Review of Obeticholic Acid, Fibrates, Seladelpar, and Elafibranor
by Fares Jamal, Amani Elshaer, Mayar H. Alatout, Nour B. Odeh, Amal Youssef, Humam Abo Abdullah, Sandra Elmasry, Tala Shahin, Hussein Abdul Nabi, Astin R. Worden, Talha A. Malik and Blanca C. Lizaola-Mayo
Biomedicines 2025, 13(10), 2335; https://doi.org/10.3390/biomedicines13102335 - 24 Sep 2025
Cited by 2 | Viewed by 4715
Abstract
Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease marked by cholestasis and progressive fibrosis. While ursodeoxycholic acid (UDCA) remains the first-line therapy, approximately 30–40% of patients have an inadequate biochemical response, increasing the risk of disease progression. Obeticholic acid (OCA), a [...] Read more.
Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease marked by cholestasis and progressive fibrosis. While ursodeoxycholic acid (UDCA) remains the first-line therapy, approximately 30–40% of patients have an inadequate biochemical response, increasing the risk of disease progression. Obeticholic acid (OCA), a potent farnesoid X receptor (FXR) agonist, was the first second-line agent approved by the only Food and Drug Administration (FDA) and has demonstrated moderate biochemical efficacy but limited tolerability due to dose-dependent pruritus and safety concerns in cirrhosis. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR-α) agonist, showed substantial alkaline phosphatase (ALP) reductions when added to UDCA, although its long-term benefit remains unconfirmed in large-scale trials and its use remains off-label in the United States, unlike FDA-approved agents. Seladelpar, a selective peroxisome proliferator-activated receptor delta (PPAR-δ) agonist, and elafibranor, a dual PPAR-α/δ agonist, have both recently received FDA accelerated approval after demonstrating significant improvements in ALP, biochemical response rates, and pruritus relief in phase 3 trials. This review summarizes these second-line therapies’ mechanisms, efficacy, safety, and limitations emphasizing the need for individualized treatment decisions and ongoing research into long-term clinical outcomes. Full article
(This article belongs to the Special Issue New Challenges in Liver Diseases: From Molecular Pathogenesis to Therapeutic Approaches)
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