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Cited by 30Liver Disease Diagnosis and TreatmentNeutrophil, Myeloperoxidase and Oxidative MechanismsLiver physiology and pathology

Neutrophils in MASLD and MASH

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Shrestha, Sanjeeb, Jeon, Jae-Han, Hong, Chang-Won·2025·BMB Reports
DOI 10.5483/bmbrep.2024-0058PMC PMC11955729
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Abstract

Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) and its progressive form, Metabolic Dysfunction Associated Steatohepatitis (MASH), represent significant health concerns associated with the metabolic syndrome. These conditions are characterized by excessive hepatic fat accumulation, inflammation, and potential progression to cirrhosis and hepatocellular carcinoma. Neutrophils are innate immune cells that play a pivotal role in the development of MASLD and MASH. They can infiltrate the hepatic microenvironment in response to inflammatory cytokines and damage associated molecular patterns (DAMPs) derived from the liver and exacerbate tissue damage by releasing of reactive oxygen species (ROS), cytokines, and neutrophil extracellular traps (NETs). Moreover, neutrophils can disrupt the metabolism of hepatocytes through key factors such as neutrophil elastase (NE) and human neutrophil peptides-1 (HNP-1), leading to inflammation and fibrosis, while myeloperoxidase (MPO) and lipocalin (LCN2) are involved in inflammatory and fibrotic processes. In contrast, neutrophils contribute to liver protection and repair through mechanisms involving microRNA-223 and matrix metalloproteinase 9 (MMP9). This dual role of neutrophils highlights their significance in the pathogenesis of MASLD and MASH. This review summarizes current understanding from recent studies on the involvement of neutrophils in MASLD and MASH. Understanding complex roles of neutrophils within the liver's unique microenvironment offers insights into novel therapeutic strategies, emphasizing the need for further research to explore neutrophil-targeted interventions for managing MASLD and MASH. [BMB Reports 2025; 58(3): 116-123].

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  • In MASLD, the hepatic immunological equilibrium is perturbed, resulting in chronic low-grade inflammation and inappropriate activation of innate and adaptive immune responses.

    “In MASLD, this finely tuned immunological equilibrium is perturbed, resulting in chronic low-grade inflammation and inappropriate activation of both innate and adaptive immune responses (Shrestha et al. 2025; Sutti and Albano 2020).”

    From The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion (2026) · cites this paper as Shrestha et al. 2025

    In “Roles of Immune Cells in MASLD and MASH Pathogenesis” (page unavailable), the paper says inflammatory responses in MASLD and MASH can disrupt the liver’s immune balance, and that chronic inflammation in MASH can dysregulate innate and adaptive immune cells. It does not characterize inflammation across MASLD as chronic low-grade inflammation, and it describes inflammation as disrupting the balance rather than the disruption causing inflammation. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Immune dysregulation critically contributes to MASLD pathogenesis.

    “growing evidence has highlighted the critical contribution of immune dysregulation to its pathogenesis.”

    From The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion (2026) · cites this paper as Shrestha et al. 2025

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Authors
Shrestha, S., Jeon, J.-H., & Hong, C.-W.
Affiliations
Kyungpook National University (KR)
Corresponding author
  • Jeon, Jae-Han
  • Hong, Chang-Won
ORCID
Venue
BMB Reports
Publisher
Korean Society for Biochemistry and Molecular Biology - BMB Reports
Published
2024-07-12
Volume
58
Issue
3
Pages
116-123
ISSN
  • 1976-6696 (ISSN-L)
  • 1976-670X
DOI
10.5483/bmbrep.2024-0058
PMC
PMC11955729
OpenAlex
W4400598504
Cited by
30
References
84
Citations by year
2026: 23 · 2025: 7
FWCI
9.15
Type
journal article
Language
en
Open access
Licence
Locations
  • BMB Reports (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Kyungpook National University Hospital
  • Korea Health Industry Development Institute
  • Ministry of Health and Welfare (HI15C0001)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
neutrophils, nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, liver inflammation, liver fibrosis, neutrophil extracellular traps, reactive oxygen species, neutrophil elastase, myeloperoxidase, neutrophil gelatinase-associated lipocalin, miR-223, MMP-9, damage-associated molecular patterns, liver regeneration, metabolic syndrome
MeSH terms
Lipocalin-2, Animals, Fatty Liver, Humans, Inflammation, Liver, Peroxidase, Neutrophils, Cytokines, Reactive Oxygen Species, Leukocyte Elastase, Matrix Metalloproteinase 9, Non-alcoholic Fatty Liver Disease

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