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Non-alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control...
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Non-alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control of Evolving Diseased States

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

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 5123

Special Issue Editor

Dr. Jérôme Eeckhoute

E-Mail Website
Guest Editor
INSERM U1011, Faculté de Médecine de Lille-Pôle Recherche, Université de Lille, Boulevard du Professeur Leclerc, Bâtiment J&K, CEDEX, 59045 Lille, France
Interests: functional genomics; transcriptional regulation; regulatory elements; transcriptomics; cell identity; liver pathophysiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fatty liver diseases have emerged as a main threat to public health, accompanying the devasting consequences of the obesity and diabetes epidemics. The range of conditions includes relatively benign lipid accumulation which can evolve to non-alcoholic steatohepatitis (NASH) characterized by liver inflammation and ultimately trigger liver fibrosis/cirrhosis. Our understanding of molecular and multicellular mechanisms underlying these various diseased states and how/why the disease evolves to more advanced states is still limited. The purpose of this Special Issue is to highlight recent findings in those areas which enlighten how NASH and associated liver fibrosis develop through modulation of the activities of different liver cell types. Submission of both reviews and original research manuscripts is welcomed.

Dr. Jérôme Eeckhoute
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. 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

  • NASH
  • fibrosis
  • disease progression
  • inflammation
  • multicellular dysfunction
  • molecular control of cell activities

Published Papers (3 papers)

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Editorial

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2 pages, 211 KiB  
Editorial
Non-Alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control of Evolving Diseased States
by Jérôme Eeckhoute
Cells 2022, 11(16), 2551; https://doi.org/10.3390/cells11162551 - 17 Aug 2022
Viewed by 1310
Abstract
Non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease, has emerged as a major threat to public health [...] Full article
(This article belongs to the Special Issue Non-alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control of Evolving Diseased States)

Research

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23 pages, 26412 KiB  
Article
Neutral Sphingomyelinase 2 Inhibition Limits Hepatic Steatosis and Inflammation
by Fatema Al-Rashed, Hossein Arefanian, Ashraf Al Madhoun, Fatemah Bahman, Sardar Sindhu, Halemah AlSaeed, Texy Jacob, Reeby Thomas, Areej Al-Roub, Fawaz Alzaid, MD Zubbair Malik, Rasheeba Nizam, Thangavel Alphonse Thanaraj, Fahd Al-Mulla, Yusuf A. Hannun and Rasheed Ahmad
Cells 2024, 13(5), 463; https://doi.org/10.3390/cells13050463 - 06 Mar 2024
Viewed by 853
Abstract
Non-alcoholic fatty liver disease (NAFLD) is manifested by hepatic steatosis, insulin resistance, hepatocyte death, and systemic inflammation. Obesity induces steatosis and chronic inflammation in the liver. However, the precise mechanism underlying hepatic steatosis in the setting of obesity remains unclear. Here, we report [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is manifested by hepatic steatosis, insulin resistance, hepatocyte death, and systemic inflammation. Obesity induces steatosis and chronic inflammation in the liver. However, the precise mechanism underlying hepatic steatosis in the setting of obesity remains unclear. Here, we report studies that address this question. After 14 weeks on a high-fat diet (HFD) with high sucrose, C57BL/6 mice revealed a phenotype of liver steatosis. Transcriptional profiling analysis of the liver tissues was performed using RNA sequencing (RNA-seq). Our RNA-seq data revealed 692 differentially expressed genes involved in processes of lipid metabolism, oxidative stress, immune responses, and cell proliferation. Notably, the gene encoding neutral sphingomyelinase, SMPD3, was predominantly upregulated in the liver tissues of the mice displaying a phenotype of steatosis. Moreover, nSMase2 activity was elevated in these tissues of the liver. Pharmacological and genetic inhibition of nSMase2 prevented intracellular lipid accumulation and TNFα-induced inflammation in in-vitro HepG2-steatosis cellular model. Furthermore, nSMase2 inhibition ameliorates oxidative damage by rescuing PPARα and preventing cell death associated with high glucose/oleic acid-induced fat accumulation in HepG2 cells. Collectively, our findings highlight the prominent role of nSMase2 in hepatic steatosis, which could serve as a potential therapeutic target for NAFLD and other hepatic steatosis-linked disorders. Full article
(This article belongs to the Special Issue Non-alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control of Evolving Diseased States)
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Other

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22 pages, 2267 KiB  
Systematic Review
The Role of Growth Hormone and Insulin Growth Factor 1 in the Development of Non-Alcoholic Steato-Hepatitis: A Systematic Review
by Luca Cristin, Amalia Montini, Alessandro Martinino, Juan Pablo Scarano Pereira, Francesco Giovinazzo and Salvatore Agnes
Cells 2023, 12(4), 517; https://doi.org/10.3390/cells12040517 - 04 Feb 2023
Cited by 4 | Viewed by 2330
Abstract
Diabetic and obese patients have a high prevalence of non-alcoholic fatty liver disease (NAFLD). This condition groups a spectrum of conditions varying from simple steatosis to non-alcoholic steatohepatitis (NASH), with or without fibrosis. Multiple factors are involved in the development of NAFLD. However, [...] Read more.
Diabetic and obese patients have a high prevalence of non-alcoholic fatty liver disease (NAFLD). This condition groups a spectrum of conditions varying from simple steatosis to non-alcoholic steatohepatitis (NASH), with or without fibrosis. Multiple factors are involved in the development of NAFLD. However, details about its pathogenesis and factors that promote the progression to NASH are still missing. Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) regulate metabolic, immune, and hepatic stellate cell functions. Increasing evidence suggests they may have roles in the progression from NAFLD to NASH. Following the PRISMA reporting guidelines, we conducted a systematic review to evaluate all clinical and experimental studies published in the literature correlating GH and IGF-1 to inflammation and fibrosis in NAFLD and NASH. Our results showed that GH and IGF-1 have a fundamental role in the pathogenesis of NASH, acting in slightly different ways to produce a synergic effect. Indeed, GH may mediate its protective effect in the pathogenesis of NASH by regulating lipogenesis pathways, while IGF-1 has the same effect by regulating cholesterol transport. Therefore, they could be used as therapeutic strategies in preventing NAFLD progression to NASH. Full article
(This article belongs to the Special Issue Non-alcoholic Steatohepatitis (NASH) and Liver Fibrosis: Molecular and Multicellular Control of Evolving Diseased States)
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