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Cited by 21Liver Disease Diagnosis and TreatmentMicroRNA in disease regulationLiver physiology and pathology

miR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression

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Fernández-Tussy, Pablo, Cardelo, Magdalena P., Zhang, Hanming, Sun, Jonathan, Price, Nathan L., Boutagy, Nabil E., Goedeke, Leigh, Cadena-Sandoval, Martí +9 more·2024·JCI Insight
DOI 10.1172/jci.insight.168476PMC PMC11466198
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Abstract

The complexity of the mechanisms underlying metabolic dysfunction–associated steatotic liver disease (MASLD) progression remains a significant challenge for the development of effective therapeutics. miRNAs have shown great promise as regulators of biological processes and as therapeutic targets for complex diseases. Here, we study the role of hepatic miR-33, an important regulator of lipid metabolism, during the progression of MASLD and the development of hepatocellular carcinoma (HCC). We report that miR-33 was elevated in the livers of humans and mice with MASLD and that its deletion in hepatocytes (miR-33 HKO ) improved multiple aspects of the disease, including steatosis and inflammation, limiting the progression to metabolic dysfunction–associated steatotic hepatitis (MASH), fibrosis, and HCC. Mechanistically, hepatic miR-33 deletion reduced lipid synthesis and promoted mitochondrial fatty acid oxidation, reducing lipid burden. Additionally, absence of miR-33 altered the expression of several known miR-33 target genes involved in metabolism and resulted in improved mitochondrial function and reduced oxidative stress. The reduction in lipid accumulation and liver injury resulted in decreased YAP/TAZ pathway activation, which may be involved in the reduced HCC progression in HKO livers. Together, these results suggest suppressing hepatic miR-33 may be an effective therapeutic approach to temper the development of MASLD, MASH, and HCC in obesity.

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  • Hepatic deletion of miR-33a reduces liver lipid content by suppressing lipid synthesis and enhancing fatty acid oxidation, improves mitochondrial function, and alleviates oxidative stress through AMPKα and PGC1α activation, leading to reduced activation of the YAP/TAZ pathway.

    “Hepatic deletion of miR-33a reduces liver lipid content by suppressing lipid synthesis and enhancing fatty acid oxidation, improves the mitochondrial function, and alleviates oxidative stress through AMPKα and PGC1α activation, leading to reduced activation of the YAP/TAZ pathway.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [37]

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  • miR-33 contributes to hepatic lipid accumulation by repressing fatty acid oxidation genes and promoting lipogenesis.

    “MiR-33 contributes to hepatic lipid accumulation by repressing fatty acid oxidation genes and promoting lipogenesis.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [37]

  • miR-33a knockout in hepatocytes reduces steatosis with improved insulin sensitivity and glucose homeostasis and suppresses the subsequent progression to MASH and hepatocellular carcinoma (HCC) by reducing the lipid burden in the liver.

    “MiR-33a knockout in hepatocytes reduces steatosis with improved insulin sensitivity and glucose homeostasis and suppresses the subsequent progression to MASH and hepatocellular carcinoma (HCC) by reducing the lipid burden in the liver 36 , 37) .”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [37]

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Authors
Fernández-Tussy, P., Cardelo, M. P., Zhang, H., Sun, J., Price, N. L., Boutagy, N. E., Goedeke, L., Cadena-Sandoval, M., Xirouchaki, C. E., Brown, W., Yang, X., Pastor-Rojo, O., Haeusler, R. A., Bennett, A. M., Tiganis, T., Suárez, Y., & Fernández-Hernando, C.
Affiliations
  • Vascular Biology and Therapeutics Program,
  • Yale University (US)
  • National Institutes of Health (US)
  • Cardiovascular Institute Hospital (JP)
  • Department of Pathology & Cell Biology and Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.
  • The Alfred Hospital (AU)
  • Monash University (AU)
  • Columbia University Irving Medical Center (US)
ORCID
Venue
JCI Insight
Publisher
American Society for Clinical Investigation
Published
2024-08-27
Volume
9
Issue
19
ISSN
2379-3708 (ISSN-L)
DOI
10.1172/jci.insight.168476
PMC
PMC11466198
OpenAlex
W4401909116
Cited by
21
References
108
Citations by year
2026: 12 · 2025: 8 · 2024: 1
FWCI
6.37
Type
journal article
Language
en
Open access
Licence
Locations
  • JCI Insight (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • NHBLI (R35HL135820, R35HL155988, R00HL150234)
  • NIDDK (1K01DK120794)
  • American Heart Association (20TPA35490416, 23CDA1055007)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
miR-33, non-alcoholic fatty liver disease, hepatocellular carcinoma, hepatocyte-specific knockout, steatosis, liver fibrosis, lipogenesis, mitochondrial fatty acid oxidation, oxidative stress, YAP/TAZ pathway, obesity, lipid metabolism, microRNA therapeutic target
MeSH terms
Animals, Disease Models, Animal, Fatty Liver, Carcinoma, Hepatocellular, Humans, Liver, Liver Neoplasms, Male, Mice, Knockout, Disease Progression, Hepatocytes, MicroRNAs, Lipid Metabolism, Mice

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