Exploring the Cellular Basis of Steatotic Liver Disease: Insights and Advances

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 May 2025) | Viewed by 705

Special Issue Editor


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Guest Editor
Department of Hepatology and Gastroenterology, Aarhus University Hospital, 99 Palle Juul-Jensens Boulevard, 8200 Aarhus, Denmark
Interests: metabolic dysfunction-associated steatotic liver disease (MASLD); inflammatory liver disease; biomarkers; liver fibrosis; macrophages
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Special Issue Information

Dear Colleagues,

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a leading cause of chronic liver disease worldwide, with its progression ranging from simple steatosis to more severe conditions such as metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, and cirrhosis. Despite its prevalence, the cellular mechanisms underlying MASLD and its progression are still not fully understood. This Special Issue of Cells aims to explore recent insights into the cellular basis of fatty liver disease, shedding light on the complex interplay between hepatocytes, hepatic stellate cells, Kupffer cells, and immune cells in the context of lipid metabolism, inflammation, and fibrosis. Furthermore, this Special Issue will highlight advanced in vitro and in vivo models and discuss novel biomarkers and potential therapeutic strategies targeting cellular pathways to mitigate disease progression.

We invite contributions that cover cellular signaling, lipid metabolism, mitochondrial dysfunction, oxidative stress, and the role of the gut–liver axis, offering new perspectives on both the pathogenesis and potential therapeutic avenues for NAFLD.

Yours faithfully,

The Guest Editor

Prof. Dr. Henning Gronbaek
Guest Editor

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Keywords

  • metabolic dysfunction-associated steatotic liver disease (MASLD)
  • hepatocytes
  • hepatic stellate cells
  • lipid metabolism
  • inflammation
  • fibrosis
  • mitochondrial dysfunction
  • Kupffer cells
  • the microbiome
  • the gut–liver axis

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Published Papers (1 paper)

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Research

18 pages, 2954 KiB  
Article
Effects of Obeticholic Acid Treatment on Primary Human Hepatocytes in a Novel Tri-Culture Model System
by Justin J. Odanga, Sharon M. Anderson, Edward L. LeCluyse, Sharon C. Presnell, Jingsong Chen and Jessica R. Weaver
Cells 2025, 14(13), 968; https://doi.org/10.3390/cells14130968 - 24 Jun 2025
Viewed by 479
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing health concern worldwide. Human cell-based in vitro culture models that retain disease-relevant phenotypic pathways and responses to assess the efficacy and liability of new therapeutics are needed. Obeticholic Acid (OCA), a Farnesoid X Receptor [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing health concern worldwide. Human cell-based in vitro culture models that retain disease-relevant phenotypic pathways and responses to assess the efficacy and liability of new therapeutics are needed. Obeticholic Acid (OCA), a Farnesoid X Receptor agonist, has been identified for MAFLD treatment, and clinically shown to have anti-inflammatory and anti-fibrotic effects. In this study, healthy and disease-origin primary human hepatocytes (PHHs) were cultured in TruVivo®, an all-human hepatic system for 14 days and treated with OCA to determine its’ effects on lipogenic, inflammatory, and fibrogenic pathways. Decreases in lipogenesis and triglyceride levels were measured in OCA treated healthy and diseased PHHs. Significant decreases in CYP3A4 activity and gene expression were quantified. Macrophage marker expression, pro-inflammatory cytokines and fibrotic markers were lowered in OCA treated diseased PHHs. CYP7A1 gene expression decreased, while BSEP gene expression increased in OCA treated healthy and diseased PHHs. Overall, OCA treatment reduced lipogenic, inflammatory, and fibrogenic markers in diseased PHHs. Differences in the potency and efficacy of OCA against different disease-relevant pathways were observed in healthy and diseased PHHs indicating divergence of key regulatory mechanisms between healthy versus diseased phenotypes. Full article
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