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Cells
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Advances in Metabolic Dysfunction-Associated Steatotic Liver Disease
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Advances in Metabolic Dysfunction-Associated Steatotic Liver Disease

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

Deadline for manuscript submissions: 25 August 2026 | Viewed by 519

Editors

Prof. Dr. David E. Stec

E-Mail Website
Guest Editor
Department of Physiology & Biophysics, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State Street, Jackson, MI 39216, USA
Interests: obesity; diabetes; hypertension; cardiovascular disease; heme oxygenase; bilirubin; biliverdin reductase; antioxidants
Special Issues, Collections and Topics in MDPI journals
Dr. Olufunto Badmus

E-Mail Website
Guest Editor
Department of Physiology & Biophysics, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State Street, Jackson, MI 39216, USA
Interests: cardiovascular disease; metabolic disorders; metabolic dysfunction-associated steatotic liver disease; gestational diabetes; bilirubin; insulin resistance; endothelial dysfunction

Special Issue Information

Dear Colleagues,

The field of non-alcoholic fatty liver disease (NAFLD), also known as hepatic steatosis, has recently garnered renewed interest due to its increasing occurrence, affecting approximately 30% of the population globally. It is described as a condition of excess fat accumulation in the liver in the presence of little or no alcohol. Due to its connection to cardiometabolic disorders such as obesity, insulin resistance, and hypertension, it was renamed metabolic dysfunction-associated steatotic liver disease (MASLD) in 2023. Hepatic steatosis is now recognized as an independent risk factor for cardiovascular disease, which is the leading cause of death. Additionally, there is a significant concern about its increasing prevalence among children and adolescents, as it is now considered the most common cause of chronic liver disease in children.

This Special issue brings together the latest advances in MASLD, highlighting mechanisms of disease pathogenesis and progression, non-invasive diagnosis, new therapeutic targets, interventions, and pediatric MASLD. Contributions include original research, review articles, and expert perspectives from leaders in hepatology and metabolism. This Special Issue seeks to serve as a crucial resource for researchers and clinicians, inspiring future discoveries that drive this field forward. 

Prof. Dr. David E. Stec
Dr. Olufunto Badmus
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • NAFLD
  • MASLD
  • hepatic steatosis
  • obesity
  • insulin resistance
  • fibrosis
  • cirrhosis

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Published Papers (1 paper)

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Research

19 pages, 38514 KB  
Article
An Integrated Analysis to Understand the Dysregulation of Innate Immune Response in Mouse Models of MASLD
by Yamini Goswami, Jyoti Gautam, Akash Baghel, Deepika Kumari, Phulwanti Kumari Sharma, M.R. Kamala Priya, Ruby Bansal, Farah Gulzar, Rajni Yadav, Guruprasad P. Aithal, Shalimar, Madhu Dikshit and Ruchi Tandon
Cells 2026, 15(14), 1298; https://doi.org/10.3390/cells15141298 - 21 Jul 2026
Viewed by 233
Abstract
Background: Dysregulation of innate immune pathways is an important contributor to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Inflammasomes serve as key regulators of innate immunity. Emerging evidence suggests that nutrient status, particularly choline, may play an important role in inflammasome [...] Read more.
Background: Dysregulation of innate immune pathways is an important contributor to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Inflammasomes serve as key regulators of innate immunity. Emerging evidence suggests that nutrient status, particularly choline, may play an important role in inflammasome activation. However, there is no systematic study across different in vitro and in vivo experiments to demonstrate the same. Methods: Hepatic expression of canonical inflammasomes such as NLRP3, NLRC4, and AIM2 and downstream inflammatory cytokines was analyzed in the high-fat-high-fructose (HF-HF) and methionine-choline-deficient (MCD) diet-induced mouse models of MASLD, along with liver biopsies from MASLD patients (n = 20). Moreover, in vitro experiments were performed to analyze the potential of choline to modulate inflammasome activation under obesogenic conditions. Results: Our data suggest increased hepatic expression of IL-1β and IL-18, at both mRNA and protein levels, in both models. While MCD-fed mice showed elevated hepatic mRNA expression of all three inflammasomes, the HF-HF diet induced a selective upregulation of NLRP3. Consistently, MCD-fed mice showed stronger induction of IL-1β and IL-18. MASLD patients also demonstrated increased hepatic expression of inflammasomes and both cytokines. In vitro, choline supplementation attenuated free fatty acid- and fructose-induced cytokine elevation. Conclusions: Our data suggest the differential activation of canonical inflammasomes across experimental MASLD models. We also observed that choline availability can serve as a potential modulator of metabolic stress-induced inflammation, highlighting the importance of nutrient status in metabolic liver disease. Full article
(This article belongs to the Special Issue Advances in Metabolic Dysfunction-Associated Steatotic Liver Disease)
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