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Biomedicines
Special Issues
Hepatotoxicity: From Pathology to Novel Therapeutic Approaches (2nd Edition)
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Hepatotoxicity: From Pathology to Novel Therapeutic Approaches (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: 31 July 2025 | Viewed by 1310

Special Issue Editor

Dr. Sanda Win

E-Mail Website
Guest Editor
Division of Gastrointestinal and Liver Disease, Department of Medicine, Keck School of Medicine, University of Southern California, 2011 Zonal Avenue, HMR 612, Los Angeles, CA 90089, USA
Interests: signal transduction in drug-induced hepatotoxicity; regulation of mitochondrial bioenergetic signaling in hepatotoxicity; metabolic dysfunction-associated steatotic liver disease (MASLD); alcoholic hepatitis; identification of therapeutic targets; cellular mechanisms of hepatotoxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatotoxicity can be caused by drug medications, chemical agents, dietary supplements, solvents, and chronic alcohol drinking. As the main organ that metabolizes and detoxifies chemicals, the liver is susceptible to the toxicity of these agents, leading to acute and chronic liver disease. Most drug-induced liver injuries (DILIs) improve after drug withdrawal, and are dose-dependent; this form of liver injury is called predictable hepatotoxicity. In other cases, liver injury is caused by unpredictable (idiosyncratic) hepatotoxicity in susceptible individuals. Active signal transduction pathways and mitochondrial dysfunction are important in determining cell survival or death. Understanding the mechanisms and signal regulation in hepatotoxicity can aid in the production of therapeutic target molecules for safe and effective treatment.

This Special Issue on hepatotoxicity aims to collect and disseminate recent findings on the mechanisms, pathophysiology, and signal transduction pathways in hepatotoxicity and advancements in therapy. Original articles, communications, and review articles are welcome.

Dr. Sanda Win
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. 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

  • cell death
  • reactive metabolites
  • oxidative stress
  • stress signaling
  • mitochondria
  • adaptive immunity
  • HLA associations
  • hepatotoxicity
  • drugs
  • liver injury
  • adverse drug reaction
  • drug-induced autoimmune hepatitis
  • idiosyncratic-drug-induced liver injury
  • bile acid
  • drug-induced cholestasis
  • hepatotoxins
  • steatosis
  • fibrosis

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Published Papers (1 paper)

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Research

21 pages, 9128 KiB  
Article
Preclinical Research on Cinnamic Acid Derivatives for the Prevention of Liver Damage: Promising Therapies for Liver Diseases
by Liseth Rubí Aldaba-Muruato, Brayan Escalante-Hipólito, Aldo Yoshio Alarcón-López, Pablo A. Martínez-Soriano, Enrique Angeles and José Roberto Macías-Pérez
Biomedicines 2025, 13(5), 1094; https://doi.org/10.3390/biomedicines13051094 - 30 Apr 2025
Viewed by 994
Abstract
Background: Liver diseases are a global health issue with an annual mortality of 80,000 patients, mainly due to complications that arise during disease progression, as effective treatments are lacking. Objectives: This study evaluated the hepatoprotective effects of two derivatives of cinnamic acid, LQM717 [...] Read more.
Background: Liver diseases are a global health issue with an annual mortality of 80,000 patients, mainly due to complications that arise during disease progression, as effective treatments are lacking. Objectives: This study evaluated the hepatoprotective effects of two derivatives of cinnamic acid, LQM717 and LQM755, in a murine model of acute liver damage induced by carbon tetrachloride (CCl4, 4 g/kg, single dose p.o.). Methods: Male Wistar rats were pretreated with five doses of LQM717 (20 mg/kg i.p.) or LQM755 (equimolar dose), starting 2 days before inducing hepatotoxic damage with CCl4. Results: The key parameters of hepatocellular function and damage showed significant increases in ALT, ALP, GGT, and total and direct bilirubin in rats intoxicated with CCl4, with decreased liver glycogen and serum albumin. Macroscopic and microscopic liver examinations revealed reduced inflammation, necrosis, and steatosis in animals pretreated with LQM717 or LQM755. Hepatomegaly was observed only in the LQM717 + CCl4 group. LQM755 statistically provided partial protection against increases in ALT and ALP and completely prevented elevations in GGT and total and direct bilirubin. LQM755 completely prevented albumin reduction, while LQM717 only partially prevented it. Both compounds partially prevented glycogen depletion. Bioinformatic analysis identified 32 potential liver protein targets for LQM717 and 36 for LQM755. Conclusions: These findings suggest that LQM717 and LQM755 have significant hepatoprotective effects against CCl4-induced acute liver injury, providing information for future studies in other acute and chronic models, as well as to elucidate their mechanisms of action. Full article
(This article belongs to the Special Issue Hepatotoxicity: From Pathology to Novel Therapeutic Approaches (2nd Edition))
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