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Chronic Liver Disease: Latest Research in Pathogenesis, Detection and Treatment, 2nd Edition

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 June 2025 | Viewed by 4244

Special Issue Editors

Dr. Cristian Turato

E-Mail Website
Guest Editor
Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy
Interests: liver cancer; liver fibrosis; NASH; liver signalling; liver models of disease; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Stefania Cannito

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy
Interests: liver disease; cancer research; liver fibrosis; metabolism and liver; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic liver diseases (CLDs) are a major challenge for global health. In patients with CLDs, liver cirrhosis and hepatocellular carcinoma (HCC) are the main contributors to morbidity and mortality, and remain a significant clinical problem. Chronic liver injuries are characterized by: 1) reiteration of liver injury and persisting inflammation as a major driving force for progressive fibrogenesis, resulting in increased deposition of extracellular matrix or ECM, eventually leading to cirrhosis and liver failure; 2) cellular levels that predominate the involvement of macrophages and Kupffer cells as well as highly proliferative, profibrogenic, migrating and contractile myofibroblast (MF)-like cells that may originate, following activation, from hepatic stellate cells (HSC/MFs). Several mechanisms can sustain fibrogenesis and its progression to advanced liver fibrosis, cirrhosis, liver failure and the development of HCC. Because of high incidence and mortality, there is a need to better understanding the mechanisms underlying the transition process from a healthy liver to end-stage disease in order to predict patients at a high risk of developing HCC, to detect HCC at an early stage and to predict evolution, recurrence and outcome after treatment.

In this Special Issue, I invite you to contribute original and cutting-edge research articles and reviews related to the title Chronic Liver Disease: Latest Research in Pathogenesis, Detection and Treatment 2.0.

More published papers could be found in the closed Special Issue: Chronic Liver Disease: Latest Research in Pathogenesis, Detection and Treatment.

Dr. Cristian Turato
Dr. Stefania Cannito
Guest Editors

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

  • NASH/NAFLD: pathogenesis, detection, and treatment
  • hepatocellular carcinoma: pathogenesis, detection, and treatment
  • inflammation in liver disease
  • 3D liver models
  • microbiota and liver disease
  • mechanisms of damage and repair: ischemia-reperfusion injury
  • cellular pathology in acute and chronic liver damage of different origin
  • biomarkers in liver disease: emerging methods and potential applications
  • immunology in the liver—from homeostasis to disease

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Published Papers (2 papers)

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Research

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13 pages, 2367 KiB  
Article
Disrupted Post-Transcriptional Regulation of Gene Expression as a Hallmark of Fatty Liver Progression
by Shohei Takaoka, Marcos E. Jaso-Vera and Xiangbo Ruan
Int. J. Mol. Sci. 2024, 25(20), 11054; https://doi.org/10.3390/ijms252011054 - 15 Oct 2024
Viewed by 1199
Abstract
It is known that both transcriptional and post-transcriptional mechanisms control messenger RNA (mRNA) levels. Compared to transcriptional regulations, our understanding of how post-transcriptional regulations adapt during fatty liver progression at the whole-transcriptome level is unclear. While traditional RNA-seq analysis uses only reads mapped [...] Read more.
It is known that both transcriptional and post-transcriptional mechanisms control messenger RNA (mRNA) levels. Compared to transcriptional regulations, our understanding of how post-transcriptional regulations adapt during fatty liver progression at the whole-transcriptome level is unclear. While traditional RNA-seq analysis uses only reads mapped to exons to determine gene expression, recent studies support the idea that intron-mapped reads can be reliably used to estimate gene transcription. In this study, we analyzed differential gene expression at both the exon and intron levels using two liver RNA-seq datasets from mice that were fed a high-fat diet for seven weeks (mild fatty liver) or thirty weeks (severe fatty liver). We found that the correlation between gene transcription and mature mRNA levels was much lower in mice with mild fatty liver as compared with mice with severe fatty liver. This result indicates broad post-transcriptional regulations for early fatty liver and such regulations are compromised for severe fatty liver. Specifically, gene ontology analysis revealed that genes involved in synapse organization and cell adhesion were transcriptionally upregulated, while their mature mRNAs were unaffected in mild fatty liver. Further characterization of post-transcriptionally suppressed genes in early fatty liver revealed that their mRNAs harbor a significantly longer 3′ UTR, one of the major features that may subject RNA transcripts to nonsense-mediated RNA decay (NMD). We further show that the expression of representative genes that were post-transcriptionally suppressed were upregulated in mice with a hepatocyte-specific defect of NMD. Finally, we provide data supporting a time-dependent decrease in NMD activity in the liver of a diet-induced metabolic-dysfunction-associated fatty liver disease mouse model. In summary, our study supports the conclusion that NMD is essential in preventing unwanted/harmful gene expression at the early stage of fatty liver and such a mechanism is lost due to decreased NMD activity in mice with severe fatty liver. Full article
(This article belongs to the Special Issue Chronic Liver Disease: Latest Research in Pathogenesis, Detection and Treatment, 2nd Edition)
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Review

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11 pages, 563 KiB  
Review
Metabolic, Inflammatory, and Molecular Impact of Cancer Cachexia on the Liver
by Daniela Caetano Gonçalves, Silvio Pires Gomes and Marília Seelaender
Int. J. Mol. Sci. 2024, 25(22), 11945; https://doi.org/10.3390/ijms252211945 - 7 Nov 2024
Cited by 1 | Viewed by 2080
Abstract
Cancer-associated cachexia (CAC) is a severe wasting syndrome, marked by involuntary weight loss and muscle wasting. It is a leading cause of cancer-related morbidity and mortality, and is driven by systemic, chronic low-grade inflammation. Key cytokines, such as IL-6 and GDF15, activate catabolic [...] Read more.
Cancer-associated cachexia (CAC) is a severe wasting syndrome, marked by involuntary weight loss and muscle wasting. It is a leading cause of cancer-related morbidity and mortality, and is driven by systemic, chronic low-grade inflammation. Key cytokines, such as IL-6 and GDF15, activate catabolic pathways in many organs. This study examined the role of inflammation and metabolic disruption in the liver during CAC, focusing on its dual role as both a target and a source of inflammatory factors. The analysis covered protein and lipid metabolism disturbances, including the hepatic production of acute-phase proteins and insulin resistance. Hepatic inflammation contributes to systemic dysfunction in CAC. The increased production of C-Reactive Protein (CRP) impacts muscle wasting, while liver inflammation leads to insulin resistance and hepatic steatosis, aggravating the cachectic state. Therefore, understanding the molecular mechanisms of liver metabolism in CAC is essential for developing effective therapies. Potential interventions include anti-inflammatory treatments, anabolic strategies, and restoration of lipid metabolism. Further research is necessary to explore the liver’s full contribution to CAC and its systemic effects, allowing to the development of liver-targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Chronic Liver Disease: Latest Research in Pathogenesis, Detection and Treatment, 2nd Edition)
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