Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.3
5.5
Journals
Biomolecules
Special Issues
Mechanisms of Nonalcoholic Liver Diseases
share announcement

Mechanisms of Nonalcoholic Liver Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 16505

Special Issue Editor

Dr. Fatiha Nassir

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA
Interests: liver; hepatocytes; enterocytes; non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); intestinal and hepatic lipid metabolism; sirtuins; mitochondria; posttranslational modifications of proteins (PMPs); liporpotein synthesis and secretion; CD36

Special Issue Information

Dear Colleagues,

Despite the progress made in understanding the pathophysiology of NAFLD, the development of pharmacological treatments for the disease has been hindered by its complexity. NAFLD implicates genetic and environmental factors, multiple organs, multiple metabolic pathways, and cross talk between different organelles in the cell. Lifestyle modifications are currently the only recommendation for the treatment of NAFLD although the mechanisms are not fully understood. The progression from NASH to advanced forms of the disease is currently an important area of research. This Special Issue welcomes contributions that address recent development in our understanding of NAFLD pathogenesis, disease mechanisms, biomarkers, current and potential pharmacological targets for treatment, lifestyle modifications, and the use of artificial intelligence in the screening and the differentiation between different stages of NAFLD. The issue accepts original research papers as well as up-to-date reviews of the literature.

Dr. Fatiha Nassir
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. Biomolecules 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 2700 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 liver disease (NAFLD)
  • Nonalcoholic steatohepatitis (NASH)
  • Pathogenesis
  • Mechanisms
  • Inflammation
  • Fibrosis
  • HCC
  • Biomarkers
  • Artificial intelligence

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

11 pages, 1658 KiB  
Article
Diagnosis of Wilson Disease and Its Phenotypes by Using Artificial Intelligence
by Valentina Medici, Anna Czlonkowska, Tomasz Litwin and Cecilia Giulivi
Biomolecules 2021, 11(8), 1243; https://doi.org/10.3390/biom11081243 - 20 Aug 2021
Cited by 6 | Viewed by 3188
Abstract
WD is caused by ATP7B variants disrupting copper efflux resulting in excessive copper accumulation mainly in liver and brain. The diagnosis of WD is challenged by its variable clinical course, onset, morbidity, and ATP7B variant type. Currently it is diagnosed by a combination [...] Read more.
WD is caused by ATP7B variants disrupting copper efflux resulting in excessive copper accumulation mainly in liver and brain. The diagnosis of WD is challenged by its variable clinical course, onset, morbidity, and ATP7B variant type. Currently it is diagnosed by a combination of clinical symptoms/signs, aberrant copper metabolism parameters (e.g., low ceruloplasmin serum levels and high urinary and hepatic copper concentrations), and genetic evidence of ATP7B mutations when available. As early diagnosis and treatment are key to favorable outcomes, it is critical to identify subjects before the onset of overtly detrimental clinical manifestations. To this end, we sought to improve WD diagnosis using artificial neural network algorithms (part of artificial intelligence) by integrating available clinical and molecular parameters. Surprisingly, WD diagnosis was based on plasma levels of glutamate, asparagine, taurine, and Fischer’s ratio. As these amino acids are linked to the urea–Krebs’ cycles, our study not only underscores the central role of hepatic mitochondria in WD pathology but also that most WD patients have underlying hepatic dysfunction. Our study provides novel evidence that artificial intelligence utilized for integrated analysis for WD may result in earlier diagnosis and mechanistically relevant treatments for patients with WD. Full article
(This article belongs to the Special Issue Mechanisms of Nonalcoholic Liver Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Research

32 pages, 1340 KiB  
Review
NAFLD: Mechanisms, Treatments, and Biomarkers
by Fatiha Nassir
Biomolecules 2022, 12(6), 824; https://doi.org/10.3390/biom12060824 - 13 Jun 2022
Cited by 88 | Viewed by 12624
Abstract
Nonalcoholic fatty liver disease (NAFLD), recently renamed metabolic-associated fatty liver disease (MAFLD), is one of the most common causes of liver diseases worldwide. NAFLD is growing in parallel with the obesity epidemic. No pharmacological treatment is available to treat NAFLD, specifically. The reason [...] Read more.
Nonalcoholic fatty liver disease (NAFLD), recently renamed metabolic-associated fatty liver disease (MAFLD), is one of the most common causes of liver diseases worldwide. NAFLD is growing in parallel with the obesity epidemic. No pharmacological treatment is available to treat NAFLD, specifically. The reason might be that NAFLD is a multi-factorial disease with an incomplete understanding of the mechanisms involved, an absence of accurate and inexpensive imaging tools, and lack of adequate non-invasive biomarkers. NAFLD consists of the accumulation of excess lipids in the liver, causing lipotoxicity that might progress to metabolic-associated steatohepatitis (NASH), liver fibrosis, and hepatocellular carcinoma. The mechanisms for the pathogenesis of NAFLD, current interventions in the management of the disease, and the role of sirtuins as potential targets for treatment are discussed here. In addition, the current diagnostic tools, and the role of non-coding RNAs as emerging diagnostic biomarkers are summarized. The availability of non-invasive biomarkers, and accurate and inexpensive non-invasive diagnosis tools are crucial in the detection of the early signs in the progression of NAFLD. This will expedite clinical trials and the validation of the emerging therapeutic treatments. Full article
(This article belongs to the Special Issue Mechanisms of Nonalcoholic Liver Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop