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Cells
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Nonalcoholic Fatty Liver Disease: From Mechanisms to Therapeutics
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Nonalcoholic Fatty Liver Disease: From Mechanisms to Therapeutics

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1343

Special Issue Editors

Dr. Stefania Di Mauro

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, 95122 Catania, Italy
Interests: NAFLD; liver; diabetes; noncoding RNAs; biomarkers; glucotoxicity; lipotoxicity; molecular biology; cell biology; lipid metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandra Scamporrino

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, 95122 Catania, Italy
Interests: NAFLD; metabolic diseases; liver; noncoding RNAs; glucotoxicity; lipotoxicity; molecular biology; cell biology; lipid metabolism; biomarkers, metabolic tissues

Special Issue Information

Dear Colleagues,

Non-alcoholic fatty liver disease (NAFLD) is the most common hepatic chronic liver disease in Western countries, with a prevalence of 20% to 30% in the general population, increasing to 70 and 90% in type 2 diabetes and obese individuals. NAFLD represents a spectrum of liver disease ranging from simple steatosis to steatosis with lobular inflammation and evidence of cellular injury (non-alcoholic steatohepatitis or NASH), liver fibrosis, cirrhosis, and hepatocellular carcinoma. The onset of simple steatosis is associated with insulin resistance and metabolic dysregulation, while in NAFLD, progression involves several pathways, including oxidative stress, fibrosis, and inflammation. Furthermore, NAFLD does not involve only the liver but other organs and tissues such as the intestine and adipose tissues. All molecular pathways involved in NAFLD onset and progression and the complex interplay among them as well as among the several impaired organs and tissues are not fully understood. Thus, the main aim of this Special Issue is to further characterize the already known mechanisms and to identify new molecular pathways dysregulated in NAFLD in order to identify novel molecular mediators that could represent future therapeutical targets.

Dr. Stefania Di Mauro
Dr. Alessandra Scamporrino
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. Cells is an international peer-reviewed open access semimonthly 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

  • NAFL
  • NASH
  • cirrhosis
  • molecular mechanisms
  • liver
  • gut
  • metabolic tissues

Published Papers (1 paper)

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Research

14 pages, 3732 KiB  
Article
In Vitro Lipid Overload Affects Cellular Proliferation, Apoptosis, and Senescence in a Time-Dependent Manner in HepG2 Hepatocytes and LX-2 Hepatic Stellate Cells
by Adriana Campos-Espinosa, Carolina Guzmán, Karla Zaira Medina-Ávila and Gabriela Gutierrez-Reyes
Cells 2024, 13(3), 282; https://doi.org/10.3390/cells13030282 - 4 Feb 2024
Viewed by 987
Abstract
Different cellular mechanisms influence steatotic liver disease (SLD) progression. The influence of different levels of steatogenic inputs has not been studied in hepatocytes and hepatic stellate cells (HSCs). Methods: HepG2 hepatocytes and LX-2 HSCs were cultured in mild (MS) and severe (SS) steatogenic [...] Read more.
Different cellular mechanisms influence steatotic liver disease (SLD) progression. The influence of different levels of steatogenic inputs has not been studied in hepatocytes and hepatic stellate cells (HSCs). Methods: HepG2 hepatocytes and LX-2 HSCs were cultured in mild (MS) and severe (SS) steatogenic conditions. TGF-β stimulation was also tested for HSCs in control (T) and steatogenic conditions (MS-T and SS-T). Steatosis was stained with Oil Red, and the proliferation was assayed via WST-8 reduction, apoptosis via flow cytometry, and senescence via SA-β-galactosidase activity. Results: Regarding hepatocytes, steatosis progressively increased; proliferation was lower in MS and SS; and the viability of both conditions significantly decreased at 72 h. Apoptosis increased in MS at 72 h, while it decreased in SS. Senescence increased in MS and diminished in SS. Regarding HSCs, the SS and SS-T groups showed no proliferation, and the viability was reduced in MS at 72 h and in SS and SS-T. The LX-2 cells showed increased apoptosis in SS and SS-T at 24 h, and in MS and MS-T at 72 h. Senescence decreased in MS, SS, and SS-T. Conclusions: Lipid overload induces differential effects depending on the cell type, the steatogenic input level, and the exposure time. Hepatocytes are resilient to mild steatosis but susceptible to high lipotoxicity. HSCs are sensitive to lipid overload, undergoing apoptosis and lowering senescence and proliferation. Collectively, these data may help explain the development of steatosis and fibrosis in SLD. Full article
(This article belongs to the Special Issue Nonalcoholic Fatty Liver Disease: From Mechanisms to Therapeutics)
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