Fatty Liver Disease: From Molecular Mechanisms to Novel Therapeutics

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 2161

Editors


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Guest Editor
Department of Internal Medicine C, Kaplan Medical Center, Rehovot 76100, Israel
Interests: alcoholic liver disease; non-alcoholic liver disease; intestinal microbiome; hepatitis C; COVID-19
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Guest Editor
In Vitro Drug Safety and Biotechnology and Department of Pharmacology and Toxicology, Faculty of Medicine, Banting Institute, University of Toronto, 100 College Street, Toronto, ON M5G 1L5, Canada
Interests: alcoholic liver disease; non-alcoholic steatohepatitis; hepatocytotoxicity; inflammatory biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The liver has a unique blood supply from both portal and systemic sources. Portal blood is delivered directly via absorption from the GI tract. This includes substances that are both ingested and produced or metabolized by the intestinal microbiome.

Hepatic steatosis is a result of either alcohol ingestion or changes in hepatic metabolism linked to metabolic syndrome, including endogenous alcohol production. Steatosis may progress via steatohepatitis, fibrosis, or cirrhosis, and its complications include hepatocellular carcinoma.

As a result of the worldwide epidemic of obesity, metabolic-associated fatty liver disease (MAFLD) is common, with a prevalence of more than 30% in developed countries. Alcohol use has also increased, linked to the COVID-19 pandemic. The combination of these two drivers has had a major effect on alcoholic and metabolic-associated fatty liver disease.

This Special Issue aims to review the cellular and molecular mechanisms that contribute to the pathogenesis of hepatic steatosis, including the clinical features, diagnosis, and management of fatty liver disease. Submissions should explore both common mechanistic systems and the involvement of the intestinal microbiome.

Dr. Stephen Malnick
Prof. Dr. Manuela G. Neuman
Guest Editors

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Keywords

  • fatty liver disease
  • metabolic-associated liver disease-MAFLD
  • alcoholic liver disease
  • non-alcoholic steatohepatitis
  • alcohol and COVID-19
  • cytokine storm
  • microbiome

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Published Papers (1 paper)

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Review

25 pages, 706 KB  
Review
Obesity, Metabolic Syndrome and MASLD in Children: Inflammation as the Missing Link—A Short Narrative Review
by Mihaela-Andreea Podeanu, Claudiu Marinel Ionele, Raluca Elena Sandu, Ion Rogoveanu, Mioara Desdemona Stepan, Carmen Elena Niculescu, Sergiu-Marian Cazacu and Ștefănița Bianca Vintilescu
Life 2026, 16(2), 310; https://doi.org/10.3390/life16020310 - 11 Feb 2026
Cited by 3 | Viewed by 1739
Abstract
Childhood obesity has emerged as a major global health challenge, with a marked increase in prevalence. Defined by excessive fat accumulation, it is associated with an increased risk of developing metabolic syndrome (MetS) and metabolic dysfunction-associated steatotic liver disease (MASLD). These conditions share [...] Read more.
Childhood obesity has emerged as a major global health challenge, with a marked increase in prevalence. Defined by excessive fat accumulation, it is associated with an increased risk of developing metabolic syndrome (MetS) and metabolic dysfunction-associated steatotic liver disease (MASLD). These conditions share common pathophysiological mechanisms, involving chronic low-grade inflammation, adipose tissue dysfunction, and insulin resistance. Excess weight contributes to the development of MetS even in the pediatric population through abdominal fat accumulation, dyslipidemia, hypertension, and hyperglycemia, while also creating a pro-inflammatory state that enhances hepatic fat accumulation, leading to MASLD. It is a bidirectional relationship, with MASLD increasing the risk of hypertension and the development of MetS individual components and as a whole. Adipose tissue, especially visceral fat, acts as a metabolic and immunologic organ, producing pro-inflammatory cytokines, which further accentuate insulin resistance and hepatic injury. The “three-strike” hypothesis illustrates the progression of MASLD. Several inflammatory biomarkers, including C-reactive protein, interleukins, adipokines, and serum ferritin, have been studied to monitor and predict disease progression in pediatrics. However, their diagnostic value in children remains limited due to age-related variability and lack of standardized pediatric cut-off points. A unified definition of pediatric MetS and MASLD is crucial to improve study comparability and clinical applicability. Such standardization would support the development of targeted strategies for early identification and intervention. Full article
(This article belongs to the Special Issue Fatty Liver Disease: From Molecular Mechanisms to Novel Therapeutics)
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