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Biology
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Cellular and Molecular Biology of Liver Diseases
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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 3225

Special Issue Editor

Dr. Matthew McMillin

E-Mail Website
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

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly 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

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

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

Published Papers (2 papers)

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Research

14 pages, 1217 KB  
Article
Effects of Bee Bread (Perga) on Pro-Inflammatory Cytokine Levels and Histopathological Alterations in the Liver and Kidneys of Streptozotocin-Induced Diabetic Rats
by Nur Akman, Turan Yaman, Ahmet Ufuk Kömüroğlu and Meryem Çalışır
Biology 2026, 15(5), 380; https://doi.org/10.3390/biology15050380 - 26 Feb 2026
Cited by 1 | Viewed by 715
Abstract
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent systemic inflammation, which contributes to progressive multi-organ dysfunction, particularly in metabolically active tissues such as the liver and kidneys. Bee bread (Perga), a fermented bee pollen product rich in bioactive compounds, has [...] Read more.
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent systemic inflammation, which contributes to progressive multi-organ dysfunction, particularly in metabolically active tissues such as the liver and kidneys. Bee bread (Perga), a fermented bee pollen product rich in bioactive compounds, has been reported to exert anti-inflammatory and organ-protective effects; however, its tissue-specific influence on inflammatory responses under diabetic conditions remains incompletely defined. Thirty-two male Wistar Albino rats were randomly assigned to four groups: Control, DM, DM + Perga, and Perga. Diabetes was induced by streptozotocin (STZ; 55 mg/kg, i.p.). Perga was administered orally at a dose of 0.5 g/kg/day for 28 days. Pro-inflammatory cytokine levels (CRP, TNF-α, IL-1β, and IL-6) were quantified in liver and kidney tissues using ELISA. Histopathological alterations were evaluated by hematoxylin and eosin staining. DM significantly increased the IL-1β, IL-6, and CRP levels in hepatic tissue and elevated TNF-α, IL-1β, IL-6, and CRP levels in renal tissue. Perga administration attenuated these inflammatory responses, particularly reducing IL-1β and IL-6 levels in the liver and all measured cytokines in the kidney. Histopathological analyses revealed hepatocyte degeneration and necrosis, sinusoidal dilatation, tubular epithelial degeneration, and glomerular damage in diabetic rats, whereas Perga treatment partially improved hepatic alterations and improved renal structural integrity. These findings indicate that Perga exerts tissue-specific anti-inflammatory and protective effects in experimental diabetes, with a more pronounced impact on renal inflammation than on hepatic responses. Although its effects on hepatic TNF-α and CRP levels were limited, Perga may act as a natural modulator of cytokine-mediated inflammatory processes. Further studies are warranted to elucidate the underlying molecular mechanisms. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology of Liver Diseases)
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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 3 | Viewed by 1870
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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