Cellular and Molecular Biology of Liver Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1169

Special Issue Editor


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Guest Editor
Department of Medicine, Baylor College of Medicine, Temple, TX 76508, USA
Interests: primary biliary cholangitis; primary sclerosing cholangitis; cholestasis; biliary atresia; autoimmune hepatitis

Special Issue Information

Dear Colleagues,

Liver diseases encompass a broad range of conditions characterized by impaired liver function due to various etiologies, including viral infections, metabolic and genetic disorders, drug toxicity, alcohol abuse, and other factors. Despite significant advances in understanding these disorders, our knowledge of the cellular and molecular mechanisms underlying many liver diseases remains incomplete. Given the limited therapeutic options currently available, it is crucial to deepen our understanding of the cellular and molecular biology driving disease progression. This knowledge is essential for identifying novel therapeutic targets and advancing treatment strategies.

For this Special Issue “Cellular and Molecular Biology of Liver Diseases”, we encourage the submission of research articles that expand our knowledge of the cellular or molecular mechanisms of liver diseases. We welcome both research articles and relevant reviews that cover the aforementioned subjects.

Dr. Matthew McMillin
Guest Editor

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Keywords

  • drug-induced liver injury
  • cholestasis
  • hepatitis
  • metabolic dysfunction-associated steatotic liver disease
  • alcohol-associated liver disease

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Published Papers (1 paper)

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Research

21 pages, 5020 KB  
Article
Divergent Hepatic and Adipose Tissue Effects of Kupffer Cell Depletion in a Male Rat Model of Metabolic-Associated Steatohepatitis
by Morena Wiszniewski, Diego Mori, Silvia I. Sanchez Puch, Camila Martinez Calejman, Cora B. Cymeryng and Esteban M. Repetto
Biology 2025, 14(8), 1058; https://doi.org/10.3390/biology14081058 - 15 Aug 2025
Cited by 1 | Viewed by 752
Abstract
Kupffer cells (KCs) play a pivotal role in the progression of metabolic-associated steatohepatitis (MASH). This study evaluated the impact of short-term KC depletion induced by gadolinium chloride (GdCl3) in a rat model of MASH. The intervention with GdCl3 effectively reduced [...] Read more.
Kupffer cells (KCs) play a pivotal role in the progression of metabolic-associated steatohepatitis (MASH). This study evaluated the impact of short-term KC depletion induced by gadolinium chloride (GdCl3) in a rat model of MASH. The intervention with GdCl3 effectively reduced KC markers CD68 and Clec4f, together with pro-inflammatory cytokines (IL-1β, TNFα, NOS2), without affecting anti-inflammatory markers (IL-10, MRC1). Histologically, GdCl3 reduced hepatocyte ballooning and NAS despite persistent steatosis. KC depletion was associated with decreased oxidative stress markers (TBARS, 3-nitrotyrosine) and antioxidant enzyme activity (SOD, catalase). Additionally, markers of endoplasmic reticulum stress (ATF4, GRP78, CHOP, P58IPK) and apoptosis (BAX/BCL2 ratio, cleaved caspase-3) were diminished. Despite these improvements, GdCl3 had no effect on lipid or glucose metabolism in the liver, associated with persistent elevation of PTP1B expression induced by SRD intake. KC depletion, however, increased FGF21 expression. GdCl3 treatment improved systemic insulin sensitivity and reduced fasting glucose and NEFA serum levels. In white adipose tissue, the treatment decreased adipocyte size, restored insulin signaling, and inhibited lipolysis (ATGL expression) without altering macrophage infiltration (IBA) or thermogenic protein levels (UCP1) in SRD rats. These findings suggest that KC depletion modulates liver-to-adipose tissue crosstalk, potentially through FGF21 signaling, contributing to improved systemic metabolic homeostasis of SRD animals. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology of Liver Diseases)
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