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Cellular and Molecular Mechanisms of Nonalcoholic Fatty Liver Disease
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Cellular and Molecular Mechanisms of Nonalcoholic Fatty Liver Disease

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 3369

Special Issue Editor

Dr. LiKang Chin

E-Mail Website
Guest Editor
Department of Biomedical Engineering, Widener University, Chester, PA 19087, USA
Interests: mechanobiology; lipids, obesity; adipocyte biology; nonalcoholic fatty liver disease; biomaterials

Special Issue Information

Dear Colleagues,

Nonalcoholic fatty liver disease (NAFLD) is a global epidemic. Affecting nearly one third of the adult population worldwide, NAFLD is the most common cause of chronic liver disease. The condition is associated with metabolic syndrome, obesity, diabetes, and cardiovascular risk.

The spectrum of NAFLD ranges from simple hepatic steatosis to the more severe case of nonalcoholic steatohepatitis (NASH), which is characterized by inflammation and cellular damage observed as hepatocellular ballooning. Although milder cases are generally benign, NAFLD can develop into more serious liver diseases such as cirrhosis and hepatocellular carcinoma.

The cellular and molecular mechanism underlying the advancement of NAFLD to more severe conditions are not completely known, but the prevailing “multi-hit” theory attributes disease progression to many insults, including impaired insulin signaling, mitochondrial dysfunction, inflammation, adipokines, and oxidative stress. Mechanical cues have also been implicated.

In this Special Issue of Current Issues in Molecular Biology, we welcome articles highlighting the cellular and molecular mechanisms underlying the development and progression of NAFLD, NASH, and related diseases.

This Special Issue is supervised by Dr. LiKang Chin (Biomedical Engineering, Widener University) and assisted by our Topical Advisory Panel Member Dr. Aylin Acun (Biomedical Engineering, Widener University).

Dr. LiKang Chin
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. Current Issues in Molecular Biology 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 2200 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

  • nonalcoholic fatty liver disease (NAFLD)
  • metabolic-associated fatty liver disease (MAFLD)
  • nonalcoholic steatohepatitis (NASH)
  • cardiovascular disease
  • hepatocellular carcinoma
  • lipotoxicity
  • inflammation
  • insulin resistance
  • obesity
  • liver fibrosis
  • reactive oxygen species

Published Papers (3 papers)

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Research

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11 pages, 1826 KiB  
Article
Identifying Candidate Polyphenols Beneficial for Oxidative Liver Injury through Multiscale Network Analysis
by Sang Yun Han, Ji-Hwan Kim, Gi-Sang Bae and Won-Yung Lee
Curr. Issues Mol. Biol. 2024, 46(4), 3081-3091; https://doi.org/10.3390/cimb46040193 - 02 Apr 2024
Viewed by 358
Abstract
Oxidative stress, a driver of liver pathology, remains a challenge in clinical management, necessitating innovative approaches. In this research, we delved into the therapeutic potential of polyphenols for oxidative liver injury using a multiscale network analysis framework. From the Phenol-Explorer database, we curated [...] Read more.
Oxidative stress, a driver of liver pathology, remains a challenge in clinical management, necessitating innovative approaches. In this research, we delved into the therapeutic potential of polyphenols for oxidative liver injury using a multiscale network analysis framework. From the Phenol-Explorer database, we curated a list of polyphenols along with their corresponding PubChem IDs. Verified target information was then collated from multiple databases. We subsequently measured the propagative effects of these compounds and prioritized a ranking based on their correlation scores for oxidative liver injury. This result underwent evaluation to discern its effectiveness in differentiating between known and unknown polyphenols, demonstrating superior performance over chance level in distinguishing these compounds. We found that lariciresinol and isopimpinellin yielded high correlation scores in relation to oxidative liver injury without reported evidence. By analyzing the impact on a multiscale network, we found that lariciresinol and isopimpinellin were predicted to offer beneficial effects on the disease by directly acting on targets such as CASP3, NR1I2, and CYP3A4 or by modulating biological functions related to the apoptotic process and oxidative stress. This study not only corroborates the efficacy of identified polyphenols in liver health but also opens avenues for future investigations into their mechanistic actions. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Nonalcoholic Fatty Liver Disease)
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15 pages, 3520 KiB  
Article
Effects of Melatonin on Liver of D-Galactose-Induced Aged Mouse Model
by Ran Lee, Won-Yong Lee and Hyun-Jung Park
Curr. Issues Mol. Biol. 2023, 45(10), 8412-8426; https://doi.org/10.3390/cimb45100530 - 17 Oct 2023
Viewed by 1413
Abstract
Melatonin, a hormone secreted by the pineal gland of vertebrates, regulates sleep, blood pressure, and circadian and seasonal rhythms, and acts as an antioxidant and anti-inflammatory agent. We investigated the protective effects of melatonin against markers of D-galactose (D-Gal)-induced hepatocellular aging, including liver [...] Read more.
Melatonin, a hormone secreted by the pineal gland of vertebrates, regulates sleep, blood pressure, and circadian and seasonal rhythms, and acts as an antioxidant and anti-inflammatory agent. We investigated the protective effects of melatonin against markers of D-galactose (D-Gal)-induced hepatocellular aging, including liver inflammation, hepatocyte structural damage, and non-alcoholic fatty liver. Mice were divided into four groups: phosphate-buffered saline (PBS, control), D-Gal (200 mg/kg/day), melatonin (20 mg/kg), and D-Gal (200 mg/kg) and melatonin (20 mg) cotreatment. The treatments were administered once daily for eight consecutive weeks. Melatonin treatment alleviated D-Gal-induced hepatocyte impairment. The AST level was significantly increased in the D-Gal-treated groups compared to that in the control group, while the ALT level was decreased compared to the melatonin and D-Gal cotreated group. Inflammatory genes, such as IL1-β, NF-κB, IL-6, TNFα, and iNOS, were significantly increased in the D-Gal aging model, whereas the expression levels of these genes were low in the D-Gal and melatonin cotreated group. Interestingly, the expression levels of hepatic steatosis-related genes, such as LXRα, C/EBPα, PPARα, ACC, ACOX1, and CPT-1, were markedly decreased in the D-Gal and melatonin cotreated group. These results suggest that melatonin suppresses hepatic steatosis and inflammation in a mouse model of D-Gal-induced aging. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Nonalcoholic Fatty Liver Disease)
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Review

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17 pages, 1484 KiB  
Review
Molecular Aspects of MAFLD—New Insights on Pathogenesis and Treatment
by Branka Filipovic, Marija Marjanovic-Haljilji, Dragana Mijac, Snezana Lukic, Suncica Kapor, Slobodan Kapor, Ana Starcevic, Dusan Popovic and Aleksandra Djokovic
Curr. Issues Mol. Biol. 2023, 45(11), 9132-9148; https://doi.org/10.3390/cimb45110573 - 15 Nov 2023
Cited by 1 | Viewed by 1142
Abstract
Metabolic-associated liver disease (MAFLD) affects up to 70% of overweight and more than 90% of morbidly obese people, and its pathogenesis is rather complex and multifactorial. The criteria for MAFLD include the presence of hepatic steatosis in addition to one of the following [...] Read more.
Metabolic-associated liver disease (MAFLD) affects up to 70% of overweight and more than 90% of morbidly obese people, and its pathogenesis is rather complex and multifactorial. The criteria for MAFLD include the presence of hepatic steatosis in addition to one of the following three criteria: overweight or obesity, presence of type 2 diabetes mellitus (T2DM), or evidence of metabolic dysregulation. If the specific criteria are present, the diagnosis of MAFLD can be made regardless of alcohol consumption and previous liver disease. The pathophysiological mechanisms of MAFLD, including inflammation, lipotoxicity, mitochondrial disfunction, and oxidative stress, as well as the impact of intestinal gut microbiota, are constantly being elucidated. Treatment strategies that are continually emerging are based on different key points in MAFLD pathogenesis. Yet, the ideal therapeutic option has still not been found and future research is of great importance, as MAFLD represents a multisystemic disease with numerous complications. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Nonalcoholic Fatty Liver Disease)
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