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Nonalcoholic Liver Disease: Mechanisms, Prevention, and Treatment
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Nonalcoholic Liver Disease: Mechanisms, Prevention, and Treatment

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: 20 December 2025 | Viewed by 3349

Special Issue Editors

Dr. Stefania Grimaudo

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Guest Editor
Section of Gastroenterology and Hepatology, Dipartimento di Promozione della Salute, University of Palermo, Palermo, Italy
Interests: liver disease; NAFLD; NASH; chronic hepatitis C; chronic hepatitis B; hepatocellular carcinoma; liver fibrosis; gene profiling; SNPs; transcriptomic analysis; GWAS
Special Issues, Collections and Topics in MDPI journals
Dr. Rosaria Maria Pipitone

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Guest Editor
Section of Gastroenterology and Hepatology, Dipartimento Di Promozione Della Salute, University of Palermo, Palermo, Italy
Interests: study of molecular mechanisms involved in MAFLD development and progression in terms of MASH and HCC; evaluation of the effects of compounds and phytonutrient administration, potentially capable of improving the lipid and glucose metabolic profiles, as well as steatosis and hepatic fibrosis, on in vitro models of continuous human hepatoma cell lines (HepG2) and hepatic stellate cells (LX2)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The globally estimated prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) is 25.2% and includes a wide spectrum of clinical features from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), characterized by necroinflammation and liver fibrosis, which is associated with high-risk complications, such as liver decompensation and hepatocellular carcinoma. MAFLD is characterized by clinical phenotipic heterogeneity due to its multifactorial etiology, which includes the presence of comorbidities (i.e. obesity, insulin resistance, type 2 diabetes mellitus), diet and behavior, but a key role in FLD inter-individual variation is played by the subject's genetic and epigenetic background. Lifestyle changes based on caloric restriction, the Mediterranean diet and physical activities are recommended for MAFLD prevention. However, currently, there are no approved therapeutics available for MAFLD, although several classes of drugs for MAFLD/MASH treatment are under development (i.e., FXR agonists, PPAR agonists). Genomic studies are revolutionizing the comprehension of MAFLD, improving patient stratifcation for clinical trials and for prognostication in the era of personalized medicine.

Dr. Stefania Grimaudo
Dr. Rosaria Maria Pipitone
Guest Editors

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Keywords

  • MAFLD
  • MASH
  • metabolic syndrome
  • steatosis
  • lipid droplets
  • SNPs
  • GWAS
  • therapeutc target
  • fatty liver
  • steatohepatitis
  • HCC
  • EpigEnetics

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Published Papers (3 papers)

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Research

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12 pages, 2404 KiB  
Article
Analysis of the Mitochondrial Dynamics in NAFLD: Drp1 as a Marker of Inflammation and Fibrosis
by Maël Padelli, Jocelyne Hamelin, Christophe Desterke, Mylène Sebagh, Raphael Saffroy, Claudio Garcia Sanchez, Audrey Coilly, Jean-Charles Duclos-Vallée, Didier Samuel and Antoinette Lemoine
Int. J. Mol. Sci. 2025, 26(15), 7373; https://doi.org/10.3390/ijms26157373 - 30 Jul 2025
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, projected to affect 55% globally by 2040. Up to one-third of NAFLD patients develop non-alcoholic steatohepatitis (NASH), with 40% progressing to fibrosis. However, there are currently few reliable tools to predict [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, projected to affect 55% globally by 2040. Up to one-third of NAFLD patients develop non-alcoholic steatohepatitis (NASH), with 40% progressing to fibrosis. However, there are currently few reliable tools to predict disease progression. Impaired mitochondrial dynamics, characterized by dysregulated fission, fusion, and mitophagy, have emerged as key events in NAFLD pathophysiology, contributing to hepatocyte death and inflammation. This study explored the transition from steatosis to NASH through transcriptomic analyses, including data from patients with steatosis and those with NASH at different fibrosis stages. By identifying a transcriptomic signature associated with disease progression, the study revealed increased expression of genes involved in mitochondrial dynamics in NASH compared to steatosis and during NASH-related fibrosis. Histological analyses highlighted the central role of Dynamin-related protein 1 (Drp1), a dynamin GTPase essential for mitochondrial fission and mitophagy. In human liver biopsies, Drp1 expression progressively increased from NAFLD to NASH and NASH-related fibrosis and cirrhosis, predominantly in Kupffer cells. These finding suggest Drp1 is a potential driver of the transition to more severe liver damage, making it a promising biomarker for NASH development and progression and a potential therapeutic target in metabolic disorders. Full article
(This article belongs to the Special Issue Nonalcoholic Liver Disease: Mechanisms, Prevention, and Treatment)
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Review

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31 pages, 2740 KiB  
Review
Lipid Accumulation and Insulin Resistance: Bridging Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease
by Xinyi Cao, Na Wang, Min Yang and Chun Zhang
Int. J. Mol. Sci. 2025, 26(14), 6962; https://doi.org/10.3390/ijms26146962 - 20 Jul 2025
Viewed by 480
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD), a recently proposed term to replace non-alcoholic fatty liver disease (NAFLD), emphasizes the critical role of metabolic dysfunction and applies broader diagnostic criteria. Diagnosis of MAFLD requires evidence of hepatic steatosis combined with obesity, type 2 diabetes [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD), a recently proposed term to replace non-alcoholic fatty liver disease (NAFLD), emphasizes the critical role of metabolic dysfunction and applies broader diagnostic criteria. Diagnosis of MAFLD requires evidence of hepatic steatosis combined with obesity, type 2 diabetes mellitus, or other metabolic dysregulation conditions, all of which significantly elevate the risk of chronic kidney disease (CKD). This review discusses the pathological mechanisms of lipid accumulation and insulin resistance in MAFLD and CKD, highlighting their mechanistic connections. Specifically, ectopic fat accumulation triggered by metabolic reprogramming, oxidative stress and inflammation induced by energy overload, modified lipids, uremic toxins, and senescence, as well as insulin resistance pathways activated by pro-inflammatory factors and lipotoxic products, collectively exacerbate simultaneous hepatic and renal injury. Moreover, interactions among hyperinsulinemia, the sympathetic nervous system, the renin–angiotensin system (RAS), and altered adipokine and hepatokine profiles further amplify insulin resistance, ectopic lipid deposition, and systemic damage. Finally, the review explores potential therapeutic strategies targeting lipid metabolism, insulin sensitivity, and RAS activity, which offer promise for dual-organ protection and improved outcomes in both hepatic and renal systems. Full article
(This article belongs to the Special Issue Nonalcoholic Liver Disease: Mechanisms, Prevention, and Treatment)
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18 pages, 1297 KiB  
Review
Metabolic Dysfunction-Associated Steatotic Liver Disease Induced by Microplastics: An Endpoint in the Liver–Eye Axis
by Ivan Šoša, Loredana Labinac and Manuela Perković
Int. J. Mol. Sci. 2025, 26(7), 2837; https://doi.org/10.3390/ijms26072837 - 21 Mar 2025
Viewed by 1417
Abstract
There is a significant, rather than just anecdotal, connection between the liver and the eyes. This connection is evident in noticeable cases such as jaundice, where the sclera has a yellow tint. But this can be seen through even more subtle indicators, such [...] Read more.
There is a significant, rather than just anecdotal, connection between the liver and the eyes. This connection is evident in noticeable cases such as jaundice, where the sclera has a yellow tint. But this can be seen through even more subtle indicators, such as molecules known as hepatokines. This relationship is not merely anecdotal; in some studies, it is referred to as the “liver–eye axis”. Ubiquitous environmental contaminants, such as microplastics (MPs), can enter the bloodstream and human body through the conjunctival sac, nasolacrimal duct, and upper respiratory tract mucosa. Once absorbed, these substances can accumulate in various organs and cause harm. Toxic substances from the surface of the eye can lead to local oxidative damage by inducing apoptosis in corneal and conjunctival cells, and irregularly shaped microparticles can exacerbate this effect. Even other toxicants from the ocular surface may be absorbed into the bloodstream and distributed throughout the body. Environmental toxicology presents a challenge because many pollutants can enter the body through the same ocular route as that used by certain medications. Previous research has indicated that the accumulation of MPs may play a major role in the development of chronic liver disease in humans. It is crucial to investigate whether the buildup of MPs in the liver is a potential cause of fibrosis, or simply a consequence of conditions such as cirrhosis and portal hypertension. Full article
(This article belongs to the Special Issue Nonalcoholic Liver Disease: Mechanisms, Prevention, and Treatment)
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