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Molecular Mechanisms and Novel Therapies of Liver Diseases
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Molecular Mechanisms and Novel Therapies of Liver Diseases

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: closed (31 October 2024) | Viewed by 8153

Special Issue Editor

Dr. Mi Kyung Park

E-Mail Website
Guest Editor
1. Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy National Cance Center, Goyang 10408, Republic of Korea
2. Department of Bio-Healthcare, Hwasung Medi-Science University, Hwaseong-si 18274, Republic of Korea
Interests: molecular mechanism; tumor microenvironment; epithelial-to-mesenchymal transition (EMT); post-translational modification (PTM); autophagy; potential therapeutic approaches; preclinical mouse models for cancers; breast cancer; liver cancer; lung cancer; pancreatic cancer; cancer progression and metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence and prevalence of acute and chronic liver disease (CLD) are on the rise globally. Liver disease encompasses a wide range of challenging conditions for which the underlying molecular mechanisms and effective pharmacological therapies are still unclear. Understanding the underlying molecular mechanisms of liver disease may reveal potential therapeutic targets. Liver diseases cover a diverse spectrum, often with complex molecular pathways and multiple epigenetic and post-translational modifications (PTMs). Interactions and remodeling between the liver's microenvironment and the extracellular matrix (ECM) also play a pivotal role in the progression of liver disease. Additionally, understanding the complex interplay between autophagy, molecular pathways, epigenetic modifications, and the microenvironment of the liver is essential for developing targeted therapies for various liver diseases. Various factors within the liver microenvironment may contribute to the development and progression of diseases.

This Special Issue titled "Molecular Mechanisms and Novel Therapies of Liver Diseases" serves as a dedicated platform for delving into a comprehensive exploration of the molecular mechanisms underpinning liver disease progression and the exploration of potential therapeutic approaches.

Your participation in this Special Issue is instrumental in propelling our collective knowledge and driving progress toward improved outcomes for individuals affected by liver disease. We eagerly anticipate your valuable contributions and insights.

Dr. Mi Kyung Park
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

  • acute and chronic liver diseases (CLDs)
  • hepatocellular carcinoma (HCC)
  • post-translational modification (PTM)
  • autophagy
  • potential therapeutic approaches
  • preclinical mouse models
 

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Published Papers (3 papers)

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Research

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16 pages, 4063 KiB  
Article
Hyperbaric Treatment Stimulates Chaperone-Mediated Macroautophagy and Autophagy in the Liver Cells of Healthy Female Rats
by Agnieszka Pedrycz, Mariusz Kozakiewicz, Mansur Rahnama, Marek Kos, Ewelina Grywalska, Marietta Bracha, Anna Grzywacz and Iwona Bojar
Int. J. Mol. Sci. 2024, 25(19), 10476; https://doi.org/10.3390/ijms251910476 - 28 Sep 2024
Viewed by 1135
Abstract
The role of autophagy goes far beyond the elimination of damaged cellular components and the quality control of proteins. It also cleanses cells from inclusions, including pathogenic viruses, and provides energy-forming components. The liver, which is an organ with increased metabolism, is made [...] Read more.
The role of autophagy goes far beyond the elimination of damaged cellular components and the quality control of proteins. It also cleanses cells from inclusions, including pathogenic viruses, and provides energy-forming components. The liver, which is an organ with increased metabolism, is made up of cells that are particularly vulnerable to damage. Therefore, detoxification of liver cells in the process of autophagy has become a very important issue clinically. The aim of this study was an immunohistochemical evaluation of proteins activated in rat liver cells at different stages of hyperbaric autophagy. The rats used for the study were randomly divided into six equivalent groups—three control groups and three experimental groups. Animals from the experimental groups were subjected to hyperbaric treatment in a hyperbaric chamber, with a pressure of 1.6 ATA for 120 min. They breathed atmospheric air. Rats were decapitated within 5 or 10 days after removal from the chamber. Immunohistochemical reactions with beclin 1, LC3B, RAB7, and HSC73 proteins were carried out on preparations made from liver slices. A three-step labeled streptavidin–biotin detection method of paraffin blocks (LSAB three-step) was used for immunohistochemical research. The results were evaluated using computer programs for morphometric analysis of microscopic images by calculating the mean surface areas occupied by a positive immunohistochemical reaction in individual groups for all antibodies tested. Increased closure of substrates in the autophagosome (beclin 1) induced late endosome transport and accelerated autophagosome maturation process (RAB7). Furthermore, a larger number of autophagosomes (LC3B) was observed in liver cells immediately after the cessation of hyperbaric activity; however, this decreased after 5 days. During this time, chaperone-mediated autophagy (HSC73) was observed on a larger scale. This means that increased macroautophagy induced by hyperbaric treatment weakens with time that has elapsed since the cessation of high pressure, whereas similarly induced chaperone-mediated autophagy intensifies over time. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies of Liver Diseases)
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Review

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23 pages, 1600 KiB  
Review
The Relationship between Pathogenesis and Possible Treatments for the MASLD-Cirrhosis Spectrum
by Paulina Vidal-Cevallos, Adriana P. Sorroza-Martínez, Norberto C. Chávez-Tapia, Misael Uribe, Eduardo E. Montalvo-Javé and Natalia Nuño-Lámbarri
Int. J. Mol. Sci. 2024, 25(8), 4397; https://doi.org/10.3390/ijms25084397 - 16 Apr 2024
Cited by 8 | Viewed by 3896
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a term that entails a broad spectrum of conditions that vary in severity. Its development is influenced by multiple factors such as environment, microbiome, comorbidities, and genetic factors. MASLD is closely related to metabolic syndrome as [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a term that entails a broad spectrum of conditions that vary in severity. Its development is influenced by multiple factors such as environment, microbiome, comorbidities, and genetic factors. MASLD is closely related to metabolic syndrome as it is caused by an alteration in the metabolism of fatty acids due to the accumulation of lipids because of an imbalance between its absorption and elimination in the liver. Its progression to fibrosis is due to a constant flow of fatty acids through the mitochondria and the inability of the liver to slow down this metabolic load, which generates oxidative stress and lipid peroxidation, triggering cell death. The development and progression of MASLD are closely related to unhealthy lifestyle habits, and nutritional epigenetic and genetic mechanisms have also been implicated. Currently, lifestyle modification is the first-line treatment for MASLD and nonalcoholic steatohepatitis; weight loss of ≥10% produces resolution of steatohepatitis and fibrosis regression. In many patients, body weight reduction cannot be achieved; therefore, pharmacological treatment should be offered in particular populations. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies of Liver Diseases)
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29 pages, 3522 KiB  
Review
Unraveling the Janus-Faced Role of Autophagy in Hepatocellular Carcinoma: Implications for Therapeutic Interventions
by Thi Ha Nguyen, Tuan Minh Nguyen, Dinh Thi Minh Ngoc, Taesik You, Mi Kyung Park and Chang Hoon Lee
Int. J. Mol. Sci. 2023, 24(22), 16255; https://doi.org/10.3390/ijms242216255 - 13 Nov 2023
Cited by 7 | Viewed by 2309
Abstract
This review aims to provide a comprehensive understanding of the molecular mechanisms underlying autophagy and mitophagy in hepatocellular carcinoma (HCC). Autophagy is an essential cellular process in maintaining cell homeostasis. Still, its dysregulation is associated with the development of liver diseases, including HCC, [...] Read more.
This review aims to provide a comprehensive understanding of the molecular mechanisms underlying autophagy and mitophagy in hepatocellular carcinoma (HCC). Autophagy is an essential cellular process in maintaining cell homeostasis. Still, its dysregulation is associated with the development of liver diseases, including HCC, which is one of leading causes of cancer-related death worldwide. We focus on elucidating the dual role of autophagy in HCC, both in tumor initiation and progression, and highlighting the complex nature involved in the disease. In addition, we present a detailed analysis of a small subset of autophagy- and mitophagy-related molecules, revealing their specific functions during tumorigenesis and the progression of HCC cells. By understanding these mechanisms, we aim to provide valuable insights into potential therapeutic strategies to manipulate autophagy effectively. The goal is to improve the therapeutic response of liver cancer cells and overcome drug resistance, providing new avenues for improved treatment options for HCC patients. Overall, this review serves as a valuable resource for researchers and clinicians interested in the complex role of autophagy in HCC and its potential as a target for innovative therapies aimed to combat this devastating disease. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies of Liver Diseases)
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