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Medicina
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Research Advances in Non-alcoholic Fatty Liver Disease
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Research Advances in Non-alcoholic Fatty Liver Disease

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Gastroenterology & Hepatology".

Deadline for manuscript submissions: closed (30 January 2023) | Viewed by 14267

Special Issue Editors

Dr. Naoto Nagata

E-Mail Website
Guest Editor
Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
Interests: NAFLD; obesity
Dr. Guanliang Chen

E-Mail Website
Guest Editor
Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
Interests: NASH; fibrosis; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There is an unmet medical need for effective pharmacotherapy for nonalcoholic fatty liver disease (NAFLD). The pathogenesis of NAFLD is complex and still unclear since NALFD is not only a hepatic manifestation of metabolic syndrome, but the inter-organ crosstalk between the liver and peripheral organs including the gut flora also involves its development. Thus, further basic research is still required to find a novel preventive or therapeutic approach.

The other challenging part is a noninvasive diagnostic modality for NASH, the progressive form of NAFLD. Liver biopsy is the gold standard in the staging and grading of NASH, but invasive and histologic scoring systems are semiquantitative with large variations between observers. Thus, noninvasive imaging and serum biomarkers are needed for accurate diagnosis and long-term monitoring of the disease status.

This Special Issue welcomes manuscripts addressing any aspects of NAFLD research. We are pleased to invite you and your colleagues to submit your original articles, from basic to clinical research, including comprehensive reviews, that present an overview of the currently available knowledge and recent findings regarding NAFLD.

Dr. Naoto Nagata
Dr. Guanliang Chen
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. Medicina is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). 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

  • NAFLD
  • NASH
  • gut flora
  • novel therapies
  • noninvasive imaging
  • biomarkers
  • tissue repair

Published Papers (4 papers)

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Research

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18 pages, 7206 KiB  
Article
Investigation of Lonicera japonica Flos against Nonalcoholic Fatty Liver Disease Using Network Integration and Experimental Validation
by Chun-Yong Sun, Pan Zhao, Pei-Zheng Yan, Jia Li and Dong-Sheng Zhao
Medicina 2022, 58(9), 1176; https://doi.org/10.3390/medicina58091176 - 30 Aug 2022
Cited by 2 | Viewed by 1875
Abstract
Background and objective: Lonicera japonica Flos (LJF) is a well-known traditional herbal medicine that has been used as an anti-inflammatory, antibacterial, antiviral, and antipyretic agent. The potent anti-inflammatory and other ethnopharmacological uses of LJF make it a potential medicine for the treatment [...] Read more.
Background and objective: Lonicera japonica Flos (LJF) is a well-known traditional herbal medicine that has been used as an anti-inflammatory, antibacterial, antiviral, and antipyretic agent. The potent anti-inflammatory and other ethnopharmacological uses of LJF make it a potential medicine for the treatment of nonalcoholic fatty liver disease (NAFLD). This research is to explore the mechanisms involved in the activity of LJF against NAFLD using network integration and experimental pharmacology. Materials and methods: The possible targets of LJF involved in its activity against NAFLD were predicted by matching the targets of the active components in LJF with those targets involved in NAFLD. The analysis of the enrichment of GO functional annotations and KEGG pathways using Metascape, followed by constructing the network of active components–targets–pathways using Cytoscape, were carried out to predict the targets. Molecular docking studies were performed to further support the involvement of these targets in the activity of LJF against NAFLD. The shortlisted targets were confirmed via in vitro studies in an NAFLD cell model. Results: A total of 17 active components in LJF and 29 targets related to NAFLD were predicted by network pharmacology. Molecular docking studies of the main components and the key targets showed that isochlorogenic acid B can stably bind to TNF-α and CASP3. In vitro studies have shown that LJF down-regulated the TNF-α and CASP3 expression in an NAFLD cell model. Conclusions: These results provide scientific evidence for further investigations into the role of LJF in the treatment of NAFLD. Full article
(This article belongs to the Special Issue Research Advances in Non-alcoholic Fatty Liver Disease)
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11 pages, 2192 KiB  
Article
Deuterium-Reinforced Polyunsaturated Fatty Acids Prevent Diet-Induced Nonalcoholic Steatohepatitis by Reducing Oxidative Stress
by Haoran Li, Ouyang Zhang, Chenmin Hui, Yaxin Huang, Hengrong Shao, Menghui Song, Lingjia Gao, Shengnan Jin, Chunming Ding and Liang Xu
Medicina 2022, 58(6), 790; https://doi.org/10.3390/medicina58060790 - 12 Jun 2022
Viewed by 2160
Abstract
Background and Objectives: Oxidative stress is implicated in the progression of nonalcoholic steatohepatitis (NASH) through the triggering of inflammation. Deuterium-reinforced polyunsaturated fatty acids (D-PUFAs) are more resistant to the reactive oxygen species (ROS)−initiated chain reaction of lipid peroxidation than regular hydrogenated (H−) PUFAs. [...] Read more.
Background and Objectives: Oxidative stress is implicated in the progression of nonalcoholic steatohepatitis (NASH) through the triggering of inflammation. Deuterium-reinforced polyunsaturated fatty acids (D-PUFAs) are more resistant to the reactive oxygen species (ROS)−initiated chain reaction of lipid peroxidation than regular hydrogenated (H−) PUFAs. Here, we aimed to investigate the impacts of D-PUFAs on oxidative stress and its protective effect on NASH. Materials and Methods: C57BL/6 mice were randomly divided into three groups and were fed a normal chow diet, a methionine–choline-deficient (MCD) diet, and an MCD with 0.6% D-PUFAs for 5 weeks. The phenotypes of NASH in mice were determined. The levels of oxidative stress were examined both in vivo and in vitro. Results: The treatment with D-PUFAs attenuated the ROS production and enhanced the cell viability in tert-butyl hydroperoxide (TBHP)−loaded hepatocytes. Concurrently, D-PUFAs decreased the TBHP-induced oxidative stress in Raw 264.7 macrophages. Accordingly, D-PUFAs increased the cell viability and attenuated the lipopolysaccharide-stimulated proinflammatory cytokine expression of macrophages. In vivo, the administration of D-PUFAs reduced the phenotypes of NASH in MCD-fed mice. Specifically, D-PUFAs decreased the liver transaminase activity and attenuated the steatosis, inflammation, and fibrosis in the livers of NASH mice. Conclusion: D-PUFAs may be potential therapeutic agents to prevent NASH by broadly reducing oxidative stress. Full article
(This article belongs to the Special Issue Research Advances in Non-alcoholic Fatty Liver Disease)
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Review

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10 pages, 780 KiB  
Review
An Update on the Chemokine System in the Development of NAFLD
by Naoto Nagata, Guanliang Chen, Liang Xu and Hitoshi Ando
Medicina 2022, 58(6), 761; https://doi.org/10.3390/medicina58060761 - 05 Jun 2022
Cited by 12 | Viewed by 4396
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. Sustained hepatic inflammation is a key driver of the transition from simple fatty liver to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. Hepatic inflammation is orchestrated [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. Sustained hepatic inflammation is a key driver of the transition from simple fatty liver to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. Hepatic inflammation is orchestrated by chemokines, a family of chemoattractant cytokines that are produced by hepatocytes, Kupffer cells (liver resident macrophages), hepatic stellate cells, endothelial cells, and vascular smooth muscle cells. Over the last three decades, accumulating evidence from both clinical and experimental investigations demonstrated that chemokines and their receptors are increased in the livers of NAFLD patients and that CC chemokine ligand (CCL) 2 and CCL5 in particular play a pivotal role in inducing insulin resistance, steatosis, inflammation, and fibrosis in liver disease. Cenicriviroc (CVC), a dual antagonist of these chemokines’ receptors, CCR2 and CCR5, has been tested in clinical trials in patients with NASH-associated liver fibrosis. Additionally, recent studies revealed that other chemokines, such as CCL3, CCL25, CX3C chemokine ligand 1 (CX3CL1), CXC chemokine ligand 1 (CXCL1), and CXCL16, can also contribute to the pathogenesis of NAFLD. Here, we review recent updates on the roles of chemokines in the development of NAFLD and their blockade as a potential therapeutic approach. Full article
(This article belongs to the Special Issue Research Advances in Non-alcoholic Fatty Liver Disease)
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16 pages, 931 KiB  
Review
Chronic Inflammation—A Link between Nonalcoholic Fatty Liver Disease (NAFLD) and Dysfunctional Adipose Tissue
by Maria Petrescu, Sonia Irina Vlaicu, Lorena Ciumărnean, Mircea Vasile Milaciu, Codruța Mărginean, Mira Florea, Ștefan Cristian Vesa and Monica Popa
Medicina 2022, 58(5), 641; https://doi.org/10.3390/medicina58050641 - 06 May 2022
Cited by 34 | Viewed by 4863
Abstract
Nonalcoholic fatty liver disease (NAFLD) is a new challenge in modern medicine, due to its high prevalence in the world. The pathogenesis of NAFLD is a complex dysmetabolic process, following the “multiple-hit” hypothesis that involves hepatocytes excessive accumulation of triglycerides, insulin resistance (IR), [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is a new challenge in modern medicine, due to its high prevalence in the world. The pathogenesis of NAFLD is a complex dysmetabolic process, following the “multiple-hit” hypothesis that involves hepatocytes excessive accumulation of triglycerides, insulin resistance (IR), increased oxidative stress, chronic low-grade inflammatory response and lipotoxicity. In this review, we provide an overview of the interrelation of these processes, the link between systemic and local inflammation and the role of dysfunctional adipose tissue (AT) in the NAFLD development. Multiple extrahepatic triggers of the pathophysiological mechanisms of NAFLD are described: nutritional deficiency or malnutrition, unhealthy food intake, the dysfunction of the liver–gut axis, the involvement of the mesenteric adipose tissue, the role of adipokines such as adiponectin, of food intake hormone, the leptin and leptin resistance (LR) and adipose tissue’s hormone, the resistin. In addition, a wide range of intrahepatic players are involved: oxidative stress, fatty acid oxidation, endoplasmic reticulum stress, mitochondrial dysfunction, resident macrophages (Kupffer cells), neutrophils, dendritic cells (DCs), B and T lymphocytes contributing to the potential evolution of NAFLD to nonalcoholic steatohepatitis (NASH). This interdependent approach to complex dysmetabolic imbalance in NAFLD, integrating relevant studies, could contribute to a better clarification of pathogenesis and consequently the development of new personalized treatments, targeting de novo lipogenesis, chronic inflammation and fibrosis. Further studies are needed to focus not only on treatment, but also on prevention strategy in NAFLD. Full article
(This article belongs to the Special Issue Research Advances in Non-alcoholic Fatty Liver Disease)
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