ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms of Human Liver Diseases: 3rd Edition

Special Issue Editor


E-Mail Website
Guest Editor
Department of Translational Medicine, University Eastern Piedmont, 28100 Novara, Italy
Interests: oxidative stress; cardiac function; mitochondrial function; aging; nitric oxide; physiology; NAFLD; microvesicles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There are many known liver diseases, the most prominent of which are virus-induced and autoimmune hepatitis, non-alcoholic fatty liver disease (NAFLD), storage diseases such as Wilson’s disease and hemochromatosis, and acute and chronic liver failure.

NAFLD, which includes steatohepatitis (in particular, non-alcoholic steatohepatitis (NASH), which should be separated from alcoholic steatohepatitis (ASH)) and steatosis, is a rising health problem worldwide. Steatosis, liver fibrosis, and cirrhosis often develop into hepatocellular carcinogenesis, frequently resulting in the need for liver transplantation, which underlines the clinical significance of this disease complex.

Wilson’s disease (which involves morbidly heightened copper accumulation) and hemochromatosis can also both result in cirrhosis. Whereas acute liver failure can have multiple origins over a short period of time, chronic liver failure is preceded by HBV, HCV, or excessive alcohol intake over a long time span.

In this Special Issue, we provide an overview of current knowledge and recent findings regarding the development, progression, molecular pathways, and mechanisms of these diseases.

Dr. Elena Grossini
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • non-alcoholic fatty liver disease (NAFLD)
  • non-alcoholic steatohepatitis (NASH)
  • alcoholic steatohepatitis (ASH)
  • Wilson’s disease
  • hemochromatosis
  • viral hepatitis
  • autoimmune hepatitis
  • hepatocellular carcinoma
  • signaling pathways
  • molecular mechanisms
  • metabolic dysfunction-associated steatotic liver disease (MASLD)
  • metabolic dysfunction-associated steatohepatitis (MASH)

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Related Special Issues

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

26 pages, 6511 KB  
Article
Cytoprotective Effects of Agomelatine on Hepatic Ischemia–Reperfusion Injury in a Rat Model
by Yilmaz Bilgic, Sami Akbulut, Oguzhan Yildirim, Onural Ozhan, Azibe Yildiz, Zeynep Erdemli, Mehmet Erman Erdemli, Adem Kose, Nigar Vardi, Yusuf Turkoz and Hakan Parlakpinar
Int. J. Mol. Sci. 2026, 27(7), 3246; https://doi.org/10.3390/ijms27073246 - 2 Apr 2026
Viewed by 475
Abstract
Hepatic ischemia–reperfusion injury (IRI) is a major cause of liver damage and is characterized by oxidative stress, inflammatory signaling, and hepatocellular apoptosis. Aim: This study investigated the hepatoprotective effects of agomelatine (AGO) administered before ischemia or at the onset of reperfusion in a [...] Read more.
Hepatic ischemia–reperfusion injury (IRI) is a major cause of liver damage and is characterized by oxidative stress, inflammatory signaling, and hepatocellular apoptosis. Aim: This study investigated the hepatoprotective effects of agomelatine (AGO) administered before ischemia or at the onset of reperfusion in a hepatic IRI model. Rats were allocated into four experimental groups: Sham, IRI, IRI+AGO, and AGO+IRI. Hepatic ischemia was induced by clamping the hepatic pedicle for 1 h followed by 1 h of reperfusion. AGO (20 mg/kg) was administered orally either before ischemia or at the onset of reperfusion. Oxidative stress markers, antioxidant enzymes, nitric-oxide-related parameters, cytokines, liver injury enzymes, and histopathological changes were evaluated. IRI increased oxidant markers and reduced antioxidant defenses. AGO treatment improved redox balance and antioxidant parameters in both treatment groups, with stronger antioxidant responses observed in the AGO+IRI group. Nitric oxide (NO)-related markers differed among groups, including changes in L-arginine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) levels, and interleukin-6 (IL-6) levels decreased following AGO administration, particularly in the AGO+IRI group. Histopathological injury and caspase-3 expression were also attenuated in AGO-treated animals. AGO attenuates hepatic IRI by improving redox balance, modulating NO metabolism, and reducing IL-6–associated signaling and apoptosis, with stronger protection when administered before ischemia. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Human Liver Diseases: 3rd Edition)
Show Figures

Figure 1

Back to TopTop