The methyltransferase MLL4 promotes nonalcoholic steatohepatitis by enhancing NF-κB signaling
Open accessAbstract
Non-alcoholic fatty liver disease (NAFLD) is a growing health problem worldwide, ranging from non-alcoholic fatty liver (NAFL) to the more severe metabolic non-alcoholic steatohepatitis (NASH). Although many studies have elucidated the pathogenesis of NAFLD, the epigenetic regulatory mechanism from NAFL to NASH remains incompletely understood. The histone H3 lysine 4 methyltransferase, MLL4 (also called KMT2D), is a critical epigenetic transcriptional coactivator that mediates overnutrition-induced steatosis in mice, but its potential role in the progression of NASH remains largely unknown. Here, we show that mice lacking the one allele of the Mll4 gene are resistant to hepatic steatosis, inflammation, and fibrosis in NASH conditions compared to wild-type controls. Transcriptome analysis of the livers of control and Mll4 +/− mice identified pro-inflammatory genes regulated by the nuclear factor kappa B (NF-κB) signaling pathway as major target genes of MLL4. We show that MLL4 binds to p65 and that MLL4 is required for NF-κB transactivation. Myeloid-specific Mll4 knockout mice showed an almost complete block of NASH, while hepatocyte-specific Mll4 knockout mice showed mild inhibition of steatosis. Pro-inflammatory M1 polarization is decreased and anti-inflammatory M2 polarization is increased in liver macrophages from myeloid-specific Mll4 knockout mice. Importantly, we show that histone H3-lysine 4 methylation mediated by the MLL4-complex plays a critical role in promoting the expression of Ccl2 in hepatocytes and M1 marker genes in macrophages. Our results demonstrate that MLL4, through the NF-κB-MLL4 regulatory axis, exacerbates steatohepatitis in the context of an inflammatory response and represents a potential therapeutic target for NASH.
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Myeloid-specific deletion of Mll4 nearly abolishes MASH pathology and promotes a shift of hepatic macrophages toward a restorative phenotype.
“Accordingly, myeloid-specific deletion of Mll4 nearly abolishes MASH pathology and promotes a shift of hepatic macrophages toward a restorative phenotype.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [14]
The Results sections on myeloid-specific Mll4 deletion report significantly reduced liver inflammation and fibrosis in MCDD-fed mice, while the macrophage-polarization Results report fewer pro-inflammatory M1 and more anti-inflammatory M2 Kupffer cells. The Discussion calls the mice resistant to MCDD-induced NASH, but the reported histology establishes amelioration rather than showing that MASH pathology was nearly abolished overall. (LLM, conf=0.83)
Experimental — accuracy not yet measuredNF-κB-dependent inflammatory genes are major downstream targets of the histone methyltransferase MLL4.
“Transcriptomic analyses further revealed that NF-κB–dependent inflammatory genes are major downstream targets of the histone methyltransferase MLL4 (14), which directly interacts with the NF-κB subunit p65 and is required for its full transcriptional activity.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [14]
MLL4 directly interacts with the NF-κB subunit p65 and is required for its full transcriptional activity.
“Transcriptomic analyses further revealed that NF-κB–dependent inflammatory genes are major downstream targets of the histone methyltransferase MLL4 (14), which directly interacts with the NF-κB subunit p65 and is required for its full transcriptional activity.”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [14]
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- Authors
- Lee, J., An, H., Kim, C.-S., & Lee, S.
- Affiliations
- Seoul National University (KR)
- Dongduk Women's University (KR)
- Corresponding author
- Lee, Seunghee
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2024-12
- Volume
- 300
- Issue
- 12
- Pages
- 107984
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC11665687
- OpenAlex
- W4404302572
- Cited by
- 8
- References
- 66
- Citations by year
- 2026: 5 · 2025: 3
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea (RS-2024-00453874, RS-2024-00339159)
- Korea Health Industry Development Institute
- Medical Research Center, Hamad Medical Corporation (NRF-2018R1A5A2024425)
- Ministry of Health and Welfare (HI17C0447)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- KMT2D, nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, NF-κB signaling, histone H3 lysine 4 methylation, hepatic steatosis, liver inflammation, liver fibrosis, hepatic macrophages, macrophage polarization, MCP-1, epigenetic regulation
- MeSH terms
- Animals, Humans, Liver, Male, Mice, Inbred C57BL, Histone-Lysine N-Methyltransferase, Signal Transduction, NF-kappa B, Mice, Knockout, Hepatocytes, Mice, Transcription Factor RelA, Non-alcoholic Fatty Liver Disease
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