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Biomedicines
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Liver Fibrosis: Molecular Mechanisms, Potential Therapeutic Targets and Clinical Biomarkers,...
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Liver Fibrosis: Molecular Mechanisms, Potential Therapeutic Targets and Clinical Biomarkers, 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 December 2025) | Viewed by 2993

Editor

Dr. Takefumi Kimura

E-Mail Website
Guest Editor
Department of Medicine, Division of Gastroenterology and Hepatology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan
Interests: liver disease; NAFLD; NASH; hepatitis; HCC
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Liver fibrosis is an important pathological condition that directly affects the prognosis of chronic liver diseases, including viral hepatitis and metabolic dysfunction-associated steatotic liver disease (MASLD). The mechanism of fibrosis formation has long been investigated. Recently, therapies targeting hepatic stellate cells (HSC) activation, fibrosis scar evolution, immunity, and cell death have been proposed. On the other hand, the development of non-invasive fibrosis biomarkers that do not require liver biopsy is underway. Serum markers such as FIB-4 and APRI, as well as US and MRI elastography, are gaining recognition. In this Special Issue, we focus on the study of cellular signals and receptors that are altered in liver fibrosis formation. Comprehensive studies summarizing potential therapeutic targets, reports of novel therapeutic targets, and discussions of the development of fibrosis biomarkers that could serve as indicators of fibrosis treatment are welcome.

Dr. Takefumi Kimura
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • liver fibrosis treatment
  • therapeutic target biomarker
  • hepatitis
  • NAFLD
  • NASH
  • MAFLD
  • HSC
  • GPCR
  • immunity cell death

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Published Papers (1 paper)

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Research

15 pages, 2493 KB  
Article
Effect of Dotinurad on Uric Acid and Hepatorenal Parameters in Steatotic Liver Disease: A Pilot Study in Japanese Patients
by Yuma Kamijo, Takanobu Iwadare, Takefumi Kimura, Kaede Fujita, Taiki Okumura, Shun-ichi Wakabayashi, Hiroyuki Kobayashi, Tomoo Yamazaki, Naoki Tanaka and Hideo Kunimoto
Biomedicines 2025, 13(11), 2716; https://doi.org/10.3390/biomedicines13112716 - 5 Nov 2025
Viewed by 2216
Abstract
Background: Dotinurad (DOT) has demonstrated beneficial metabolic effects in preclinical models as a selective uric acid reabsorption inhibitor. However, its clinical impact on steatotic liver disease (SLD) with hyperuricemia (HU-SLD) remains unclear. Methods: This observational pilot study evaluated 33 patients with HU-SLD (Metabolic [...] Read more.
Background: Dotinurad (DOT) has demonstrated beneficial metabolic effects in preclinical models as a selective uric acid reabsorption inhibitor. However, its clinical impact on steatotic liver disease (SLD) with hyperuricemia (HU-SLD) remains unclear. Methods: This observational pilot study evaluated 33 patients with HU-SLD (Metabolic dysfunction-associated steatotic liver disease: n = 20; Metabolic dysfunction-associated alcohol-related liver disease: n = 1; Alcohol-related liver disease: n = 12) treated with DOT for at least 6 months. Laboratory parameters were assessed at baseline and at 6 months. The primary outcomes were changes in serum uric acid levels, hepatobiliary function markers, and renal function markers. Results: DOT significantly reduced serum uric acid levels from 8.4 (7.7–9.0) to 6.0 (5.9–6.8) mg/dL at 6 months (p < 0.001). Regarding hepatobiliary markers, gamma-glutamyl transferase decreased from 47 (30–78) to 43 (27–54) U/L (p = 0.042) and total bilirubin decreased from 0.6 (0.5–1.0) to 0.6 (0.4–0.7) mg/dL (p = 0.023). Significant but modest improvements in renal function were also observed, with serum creatinine decreasing from 1.1 (0.9–1.3) to 1.0 (0.9–1.1) mg/dL (p = 0.010) and estimated glomerular filtration rate increasing from 55.6 (44–67.3) to 56.6 (48.8–71.5) mL/min/1.73 m2 (p = 0.007). No significant changes were observed for aspartate aminotransferase, alanine aminotransferase, fibrosis-related markers, lipid profiles, or glycemic markers. Moreover, no treatment discontinuations or adverse events were recorded during the study period. Conclusions: DOT effectively reduced serum uric acid and modestly improved renal and hepatobiliary parameters in HU-SLD without any patient-reported complications. These real-world findings support the potential of DOT as a well-tolerated therapeutic option beyond urate lowering and warrant further investigation in larger, controlled studies. Full article
(This article belongs to the Special Issue Liver Fibrosis: Molecular Mechanisms, Potential Therapeutic Targets and Clinical Biomarkers, 2nd Edition)
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