Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.3
5.6
Journals
Biomolecules
Special Issues
Molecular Mechanisms Underlying Liver Diseases: 2nd Edition
share announcement

Molecular Mechanisms Underlying Liver Diseases: 2nd Edition

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 3371

Editor

Dr. Wei Zhong

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160, USA
Interests: alcohol-associated liver disease; gut microbiota; lipid metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a very successful first run, we are pleased to announce the launch of a second edition of a Special Issue on liver diseases.

The liver, a central metabolic hub in the human body, plays a pivotal role in maintaining homeostasis and overall health. As an organ of paramount importance, the liver is susceptible to a myriad of diseases, necessitating a comprehensive exploration of the underlying molecular mechanisms. This Special Issue aims to decipher the underlying molecular landscapes governing liver diseases, shedding light on novel insights and potential therapeutic avenues.

This collection of articles aims at addressing a diverse spectrum of liver disorders, encompassing metabolic conditions such as alcohol-associated liver disease and metabolic-associated fatty liver disease, along with viral infections and hepatocellular carcinoma. Our goal is to provide a multifaceted examination of these liver-related pathologies, offering valuable insights into their molecular mechanisms. Furthermore, we recognize the liver not in isolation but as a dynamic organ that engages in constant crosstalk with other physiological systems. Investigating the dynamic interactions between the liver and other organs is integral to our endeavor, as these interactions play a pivotal role in shaping the overall impact of liver diseases on the body. This Special Issue seeks to foster a nuanced understanding of the interplay between molecular factors, genetic determinants, and organ–organ interactions, aiming to contribute meaningfully to the field of hepatic pathophysiology.

In summary, this collection serves as a comprehensive exploration of liver diseases, aiming to unravel the complex tapestry of molecular mechanisms underlying their etiology, progression, and potential therapeutic interventions.

Dr. Wei Zhong
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. 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.

Keywords

  • pathogenesis of liver diseases
  • molecular mechanisms
  • organelle damages
  • genetic determinants
  • organ–organ interactions
  • biomarkers
  • in vivo models of liver diseases
  • therapeutic insights

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

18 pages, 5016 KB  
Article
Naringin Attenuates Steatosis, Oxidative Stress, Inflammation, and Fibrosis in MASH: Network Pharmacology and In Vivo Study
by Ji-Han Kim, Seung-Hoon Yoo, Yeon-Joo Yoo and Byung-Cheol Lee
Biomolecules 2026, 16(5), 651; https://doi.org/10.3390/biom16050651 - 27 Apr 2026
Viewed by 761
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive stage of metabolic dysfunction-associated steatotic liver disease characterized by lipid dysregulation, oxidative stress, inflammation, and fibrosis. Because these processes occur simultaneously, compounds targeting multiple pathways may offer therapeutic benefit. Naringin, a citrus-derived flavonoid, has reported antioxidant [...] Read more.
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive stage of metabolic dysfunction-associated steatotic liver disease characterized by lipid dysregulation, oxidative stress, inflammation, and fibrosis. Because these processes occur simultaneously, compounds targeting multiple pathways may offer therapeutic benefit. Naringin, a citrus-derived flavonoid, has reported antioxidant and anti-inflammatory properties, but its integrated effects in MASH remain unclear. In this study, the effects of naringin were evaluated using combined in silico analysis and in vivo experiments. Network pharmacology and molecular docking predicted targets related to lipid metabolism, oxidative stress, inflammation, and fibrosis, which were validated in a methionine- and choline-deficient diet-induced mouse model. Naringin reduced hepatic lipid accumulation and improved serum AST and ALT levels. It modulated oxidative stress-related genes, attenuated inflammatory responses, and reduced fibrogenic markers. Naringin also decreased Ly6Chigh inflammatory monocytes and Kupffer cell activation, and reduced hypothalamic microglial activation. These findings suggest that naringin exerts multi-target effects across hepatic, systemic, and central pathways, supporting its potential as a therapeutic candidate for MASH. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Liver Diseases: 2nd Edition)
►▼ Show Figures

Graphical abstract

21 pages, 3101 KB  
Article
Ezetimibe Normalizes Dietary Cholesterol-Induced Exacerbation of Liver Injury in Alcohol-Fed Mice
by Yanchao Xu, Nan Zhang, Piumi B. Wickramasinghe, Kavya Veera, Preethi Parupalli, Alex Dao, Junyu Liu, Rithika Anand, Lyndsey E. Langley, Sreeja Eadha, Hasan Iqbal, Chen Liu, Fang Bian and Lin Jia
Biomolecules 2026, 16(4), 590; https://doi.org/10.3390/biom16040590 - 16 Apr 2026
Viewed by 843
Abstract
Interactions between alcohol and nutrition play an important role in the development and progression of alcohol-associated liver disease (ALD). Although dietary cholesterol was shown to exacerbate fatty liver and liver injury in alcohol-fed mice, findings regarding the combined effect of dietary cholesterol and [...] Read more.
Interactions between alcohol and nutrition play an important role in the development and progression of alcohol-associated liver disease (ALD). Although dietary cholesterol was shown to exacerbate fatty liver and liver injury in alcohol-fed mice, findings regarding the combined effect of dietary cholesterol and heavy alcohol drinking on cholesterol homeostasis remain controversial. Ezetimibe has been widely used as a cholesterol-lowering drug in hypercholesterolemic subjects. It is not fully understood whether ezetimibe blunts the adverse effect of cholesterol on lipid and biliary bile acid metabolism in alcohol-exposed mice. In the current study, wild-type mice were subjected to NIAAA alcohol feeding model. Dietary cholesterol (0.2%, w/v) and ezetimibe (0.001%, w/v) were added to the liquid diets. Cholesterol and triglyceride contents in the liver and circulation were determined. Biliary bile acid composition, as well as hepatic and circulating inflammatory markers were analyzed. We found that ezetimibe protected mice from the synergistic effects of dietary cholesterol and alcohol on hepatic triglyceride accumulation, which was accompanied by enhanced expression of genes involved in hepatic beta oxidation. Dietary cholesterol caused great increases in liver cholesterol content and dramatic reductions in the expression of hepatic cholesterol biosynthetic genes in both control- and alcohol-fed mice. These changes were normalized by ezetimibe treatment. Ezetimibe attenuated dietary cholesterol-induced elevations in total biliary bile acids. Moreover, mice fed a diet containing both cholesterol and alcohol exhibited increased expression of monocyte chemoattractant protein 1 (Mcp1) and tumor necrosis factor alpha (Tnfα) in the distal small intestine. Collectively, our findings indicate that ezetimibe effectively mitigates the adverse effects of dietary cholesterol and alcohol consumption on hepatic lipid accumulation and liver injury. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Liver Diseases: 2nd Edition)
►▼ Show Figures

Figure 1

Review

Jump to: Research

23 pages, 3054 KB  
Review
Peroxisomes in Liver Diseases: From Metabolite Quality Control to Inter-Organelle and Inter-Organ Signaling
by Carolina Hogerty, Yantao Zhao, Weiran Wang, Steven A. Weinman and Wei Zhong
Biomolecules 2026, 16(6), 895; https://doi.org/10.3390/biom16060895 - 17 Jun 2026
Viewed by 412
Abstract
Peroxisomes are essential metabolic organelles that support core aspects of cellular homeostasis. In the hepatocytes, peroxisomes govern key aspects of cellular homeostasis, including processing lipid substrates that are inadequately handled by mitochondria, controlling hydrogen peroxide metabolism, and regulating bile acid synthesis. Increasing evidence [...] Read more.
Peroxisomes are essential metabolic organelles that support core aspects of cellular homeostasis. In the hepatocytes, peroxisomes govern key aspects of cellular homeostasis, including processing lipid substrates that are inadequately handled by mitochondria, controlling hydrogen peroxide metabolism, and regulating bile acid synthesis. Increasing evidence indicates that these organelles are not merely auxiliary metabolic compartments but active contributors to the development and progression of liver disease. Dynamic alterations in peroxisomal proteins and function are being noted. Across metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic disorders, fibrosis, and hepatocellular carcinoma, peroxisomes undergo remodeling that shows a change from adaptive reactions to maladaptive states. These changes perturb signaling pathways that regulate inflammation, stress responses, and cell fate. In addition, because peroxisomes operate within an interconnected organelle network, their dysfunction propagates to mitochondria, endoplasmic reticulum, and other cellular systems, amplifying metabolic and cellular stress. This review summarizes current understanding of how peroxisomal pathways contribute to liver disease, highlighting mechanisms involving lipid accumulation, oxidative stress, and disrupted organelle crosstalk. How peroxisome-dependent control of circulating metabolites links hepatic injury to extrahepatic organ systems is further discussed. At the end, emerging therapeutic strategies for liver disease targeting peroxisomal pathways are discussed. Together, the emerging understanding of peroxisomal remodeling, metabolic regulation, organelle crosstalk, and inter-organ communication positions peroxisomes as active and dynamic regulators of liver disease and potential targets for therapeutic intervention. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Liver Diseases: 2nd Edition)
►▼ Show Figures

Figure 1

26 pages, 594 KB  
Review
Emerging Therapeutic Perspectives in Obese Patients with MASLD Leading to Compensated Advanced Chronic Liver Disease
by Roberta Chianetta, Lydia Giannitrapani, Alessio Giuseppe Lipari, Assunta Brunone, Claudia Cannizzo, Roberto Citarrella, Maurizio Soresi, Antonio Liguori, Nadia Panera, Filomena Morisco, Luca Miele and Anna Licata
Biomolecules 2026, 16(6), 797; https://doi.org/10.3390/biom16060797 - 28 May 2026
Viewed by 577
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is now recognized as the principal hepatic manifestation of obesity and metabolic dysfunction. Its pathogenesis is complex and multifactorial, driven by insulin resistance, low-grade chronic inflammation, oxidative stress, gut microbiota alterations, and abnormalities in lipid metabolism; together, [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is now recognized as the principal hepatic manifestation of obesity and metabolic dysfunction. Its pathogenesis is complex and multifactorial, driven by insulin resistance, low-grade chronic inflammation, oxidative stress, gut microbiota alterations, and abnormalities in lipid metabolism; together, these promote steatosis, lipotoxicity, and progression to fibrosis which can lead to compensated advanced chronic liver disease (cACLD). MASLD is also a multisystem condition closely associated with an increased risk of major adverse cardiovascular events such as myocardial infarction, ischemic stroke, atrial fibrillation, and other extrahepatic complications. In this context, emerging metabolic therapies show significant potential for modifying the natural history of the disease. Glucagon-like peptide (GLP)-1 receptor agonists induce substantial weight loss and improve steatosis and necro-inflammatory activity. Sodium–glucose cotransporter 2 inhibitors (SGLT-2I) reduce glucotoxicity, promote modest weight loss, and lower hepatic fat content by improving insulin sensitivity and inflammatory signaling. Even more promising are dual GLP-1/GIP receptor agonists, which have demonstrated superior efficacy in metabolic control, reducing hepatic steatosis, and potentially modulating fibrotic processes, although definitive histological confirmation is still lacking. Overall, in this review, we discuss the physiopathological mechanisms of MASLD leading to cACLD along with the emerging therapies, such GLP1 receptor agonists, SGLT-2I, and GLP1/GIP which, when combined with structured lifestyle interventions, may attenuate progression toward steatohepatitis (MASH), fibrosis, and, thus, cirrhosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Liver Diseases: 2nd Edition)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop