Recent Advances in the Diagnosis and Treatment of Chronic Liver Diseases 2023
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 25 July 2024 | Viewed by 5734
Special Issue Editor
Interests: viral hepatitis; liver cirrhosis; portal hypertension; ascites; esophageal varices; liver fibrosis; hepatocellular carcinoma
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Chronic liver diseases develop through a wide range of causes, including hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, alcoholic-related liver disease, non-alcoholic fatty liver disease (NAFLD), and autoimmune liver diseases. Due to recent advancements in antiviral therapies and changes in lifestyle, the clinical importance of non-viral chronic liver diseases is increasing. However, viral hepatitis is a major cause of chronic liver diseases.
Recent advances in molecular and cellular techniques have succeeded in providing new perspectives related to the diagnosis and treatment of chronic liver diseases.
This Special Issue aims to cover the state-of-the-art research on chronic liver diseases. We invite authors to submit original articles, as well as review articles regarding recent findings about chronic liver diseases. We are particularly interested in molecular approaches for the diagnosis and treatment of chronic liver diseases. Potential topics include, but are not limited to, the following:
- Biomarkers for chronic liver diseases.
- Genomic researches for chronic liver diseases, including gene SNPs (single nucleotide polymorphisms).
- Molecular mechanisms of chronic liver diseases.
- Recent advances in the management of chronic liver diseases, including liver cirrhosis.
- Molecularly targeted therapy for liver cancer.
Dr. Hirayuki Enomoto
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. 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
- biomarker
- genomic research
- epigenomic research
- molecular mechanisms
- viral hepatitis
- alcoholic-related liver disease
- non-alcoholic fatty liver disease
- autoimmune liver diseases
- liver cirrhosis
- hepatocellular carcinoma
Planned Papers
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
1. Title: Alcohol- and Low-iron Induced Changes in Antioxidant and Energy Metabolism Associated with Protein Lys Acetylation
Author: Jesse A. Thornton, Zeynep C. Koc, Vincent E. Sollars, Monica A. Valentovic, James Denvir, John Wilkinson IV* and Emine C. Koc*
Abstract: Understanding the role of iron in ethanol-derived hepatic stress could help elucidate the efficacy of dietary or clinical interventions designed to minimize liver damage from chronic alcohol consumption. We hypothesized that normal levels of iron are involved in ethanol-derived liver damage and reduced dietary iron intake would lower the damage caused by ethanol. We used a pair-fed mouse model utilizing basal Lieber-DeCarli liquid diets for 22 weeks to test this hypothesis. In our mouse model, chronic ethanol exposure led to mild hepatic stress possibly characteristic of early-stage alcoholic liver disease, seen as increases in liver-to-body weight ratios. Dietary iron restriction caused a slight decrease in non-heme iron and ferritin (FeRL) expression and increased transferrin receptor 1 (TfR1) expression. It also elevated protein lysine acetylation to a more significant level than in ethanol-fed mice under normal dietary iron conditions. Interestingly, iron restriction led to an additional reduction in NAD+ and NADH levels. Consistent with this observation, the major mitochondrial NAD+-dependent deacetylase, SIRT3, was significantly reduced while the cytosolic SIRT2 expression increased in ethanol-fed mice at normal and low-iron conditions. In addition, the detection of superoxide dismutase 1 and 2 levels, SOD1 and SOD2, and oxidative phosphorylation (OXPHOS) complex activities allowed us to evaluate the changes in antioxidant and energy metabolism regulated by ethanol consumption at normal and low-iron conditions. We observed in C57BL/6J mice fed normal iron levels that mild ethanol-related liver damage was associated with reduced energy and antioxidant metabolism. Surprisingly, we found iron restriction may exacerbate certain activities of ethanol, such as the generation of protein lysine acetylation and decreasing antioxidant metabolism. This metabolic change may prove a barrier to the effectiveness of dietary reduction of iron intake as a preventative measure in chronic alcohol consumption.
2. Title: Liver Fibrosis: From beginning to therapeutic targets
Author: Dr. Pollo-Flores