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Chronic Liver Disease: From Pathophysiology to Treatment
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Chronic Liver Disease: From Pathophysiology to Treatment

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: 20 September 2025 | Viewed by 2550

Special Issue Editor

Dr. Jong-Won Kim

E-Mail Website
Guest Editor
1. Biosafety Research Institute and Laboratory of Pathology, College of Veterinary Medicine, Jeonbuk National University, Iksan 54596, Jeollabuk-do, Republic of Korea
2. Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, PA 15261, USA
Interests: paracetamol; toxic hepatitis; dose-response relationship; Crassulaceae; plant extract; antioxidant capacity

Special Issue Information

Dear Colleagues,

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health concern. It affects approximately 30% of adults in the general population, 70% of individuals with type 2 diabetes (T2D) mellitus, and nearly all patients with obesity. Notably, MASLD has become the second leading indication for liver transplantation in the United States. Over the past few decades, it has been increasingly recognized that MASLD is linked not only to serious liver-related complications but also to significant metabolic, cardiovascular, and renal issues.

Although the pathogenesis of MASLD is multifaceted, it has been well established that MASLD is closely tied to insulin resistance, abdominal obesity, and T2D. Reflecting this evidence, in 2020, the terminology was revised from non-alcoholic fatty liver disease (NAFLD) to MASLD, accompanied by an updated definition of the disease. However, regardless of the term used, NAFLD/MASLD remains a dynamic condition, shaped by a range of evolving factors. The development of specific NAFLD/MASLD phenotypes is broadly influenced by environmental triggers, genetic susceptibility, and metabolic dysfunction.

Metabolic dysfunction-associated steatohepatitis (MASH), a more severe form of MASLD, is characterized by liver inflammation and fibrosis. MASH is particularly concerning due to its progression towards cirrhosis and liver failure, further underscoring the need for early identification and intervention.

This Special Issue of the International Journal of Molecular Sciences will highlight recent advances in the understanding of NAFLD/MASLD and MASH, including novel insights into their pathogenesis and treatment. It will feature a selection of cutting-edge research and comprehensive review articles focused on the molecular mechanisms and therapeutic strategies for NAFLD/MASLD and MASH. We welcome experimental studies, up-to-date review articles, and commentaries on emerging topics in this field.

Dr. Jong-Won Kim
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.

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Keywords

  • nonalcoholic fatty liver disease (NAFLD)
  • metabolic dysfunction-associated steatotic liver disease (MASLD)
  • metabolic dysfunction-associated steatohepatitis (MASH)
  • type 2 diabetes (T2D)

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Published Papers (3 papers)

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Research

18 pages, 4146 KiB  
Article
Identification and Assessment of lncRNAs and mRNAs in PM2.5-Induced Hepatic Steatosis
by Peixuan Tian, Hui Xia, Xinbao Li, Ying Wang, Bihuan Hu, Yu Yang, Guiju Sun and Jing Sui
Int. J. Mol. Sci. 2025, 26(6), 2808; https://doi.org/10.3390/ijms26062808 - 20 Mar 2025
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Abstract
Research indicates that fine particulate matter (PM2.5) exposure is associated with the onset of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disorder. However, the underlying pathogenesis mechanisms remain to be fully understood. Our study investigated the hub long non-coding RNAs [...] Read more.
Research indicates that fine particulate matter (PM2.5) exposure is associated with the onset of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disorder. However, the underlying pathogenesis mechanisms remain to be fully understood. Our study investigated the hub long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) associated with hepatic steatosis caused by PM2.5 exposure and their pathological mechanisms. The analysis of gene profiles in the GSE186900 dataset from the Gene Expression Omnibus (GEO) enabled the identification of 38 differentially expressed lncRNAs and 1945 mRNAs. To explore further, a co-expression network was established utilizing weighted gene co-expression network analysis (WGCNA). Moreover, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were utilized for functional enrichment analysis. Our analysis identified specific modules, particularly the blue and turquoise modules, which showed a strong correlation with NAFLD. Through functional enrichment analysis, we identified several lncRNAs (including Gm15446, Tmem181b-ps, Adh6-ps1, Gm5848, Zfp141, Rmrp, and Rb1) which may be involved in modulating NAFLD, multiple metabolic pathways, inflammation, cell senescence, apoptosis, oxidative stress, and various signaling pathways. The hub lncRNAs identified in our study provide novel biomarkers and potential targets for the diagnosis and treatment of NAFLD. Full article
(This article belongs to the Special Issue Chronic Liver Disease: From Pathophysiology to Treatment)
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15 pages, 19434 KiB  
Article
Identification of a Novel NPC1L1 Inhibitor from Danshen and Its Role in Nonalcoholic Fatty Liver Disease
by Donghai Xia, Xuan Jiang, Xiaomin Xie, Han Zhou, Dongping Yu, Gaowa Jin, Xianlong Ye, Shenglong Zhu, Zhimou Guo and Xinmiao Liang
Int. J. Mol. Sci. 2025, 26(6), 2793; https://doi.org/10.3390/ijms26062793 - 20 Mar 2025
Viewed by 422
Abstract
Danshen, a well-known traditional Chinese medicine (TCM), has gained increasing attention for its protective effects on nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms underlying these effects remain to be elucidated. Niemann-Pick C1-like 1 (NPC1L1), a key transporter mediating intestinal cholesterol absorption, [...] Read more.
Danshen, a well-known traditional Chinese medicine (TCM), has gained increasing attention for its protective effects on nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanisms underlying these effects remain to be elucidated. Niemann-Pick C1-like 1 (NPC1L1), a key transporter mediating intestinal cholesterol absorption, has emerged as a critical target for NAFLD treatment. This study aimed to screen for NPC1L1 inhibitors from Danshen and investigate their therapeutic effects on NAFLD. We established a high-throughput screening platform using stable Caco2 cell lines expressing human NPC1L1 (hL1-Caco2) and discovered that tanshinones (Tans), the liposoluble components of Danshen, inhibited NPC1L1-mediated cholesterol absorption in hL1-Caco2 cells. Additionally, Tans treatment reduced hepatic steatosis in high-fat diet (HFD)-fed mice. To identify the active compounds in Tans, activity-oriented separation was performed by integrating the high-throughput screening platform and two-dimensional chromatographic techniques. Ultimately, cryptotanshinone (CTS) was identified as a novel NPC1L1 inhibitor and significantly decreased hepatic steatosis in HFD-fed mice. Molecular docking and dynamics simulation showed that CTS stably bound with NPC1L1, where TRP383 acted as the key amino acid. Taken together, this study demonstrates, for the first time, that CTS, a liposoluble compound from Danshen, is a novel NPC1L1 inhibitor. Our findings suggest that the inhibitory effect of CTS against NPC1L1-mediated intestinal cholesterol absorption may be a potential mechanism, contributing to its alleviation of NAFLD in mice. Full article
(This article belongs to the Special Issue Chronic Liver Disease: From Pathophysiology to Treatment)
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16 pages, 4684 KiB  
Article
Establishing the Role of Liver Fatty Acid-Binding Protein in Post-Golgi Very-Low-Density Lipoprotein Trafficking Using a Novel Fluorescence-Based Assay
by Kayli Winterfeldt, Fahim Rejanur Tasin and Shadab A. Siddiqi
Int. J. Mol. Sci. 2025, 26(6), 2399; https://doi.org/10.3390/ijms26062399 - 7 Mar 2025
Viewed by 1215
Abstract
The liver plays a crucial role in maintaining lipid homeostasis by converting toxic free fatty acids into VLDL, which the body uses for energy. Even minor changes in VLDL formation and secretion can result in serious health conditions such as atherosclerosis and non-alcoholic [...] Read more.
The liver plays a crucial role in maintaining lipid homeostasis by converting toxic free fatty acids into VLDL, which the body uses for energy. Even minor changes in VLDL formation and secretion can result in serious health conditions such as atherosclerosis and non-alcoholic fatty liver disease. Despite the importance of VLDL, the proteins and signaling pathways involved in its regulation remain largely unknown. This study aims to develop a novel methodology to study intracellular VLDL transport events and explore the role of liver fatty acid-binding protein (LFABP) in VLDL transport and secretion. Current methods to study VLDL are often tedious, time-consuming, and expensive, underscoring the need for an alternative approach. We designed a new immunofluorescence-based assay to track the formation and secretion of VLDL in cells over time using fluorescently tagged TopFluor oleic acid. Confocal microscopy confirmed that TopFluor oleic acid enters hepatocytes and colocalizes with the ER, Golgi, and plasma membrane. Additionally, the collection of cell culture media revealed that TopFluor was incorporated into VLDL particles, as confirmed by fluorescence readings and ApoB100 immunoblots. This novel assay provides a valuable tool for further research into the mechanisms of VLDL regulation and the development of potential therapeutic targets for related diseases. Utilizing this assay, we identified LFABP as a key regulatory protein in post-Golgi VLDL trafficking. Our data suggest that LFABP plays a crucial role in this process, and its functional impairment leads to reduced VLDL secretion. Full article
(This article belongs to the Special Issue Chronic Liver Disease: From Pathophysiology to Treatment)
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