ArticleJCI insight2024
miR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed.
- Context-dependent regulation of endothelial inflammation and atherosclerosis by endothelial microRNA-33.Atherosclerosis · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- OCTN2 Activates a Non-Canonical Carnitine Metabolic Pathway to Promote MASH-HCC Progression and Immunotherapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roles of Extracellular Vesicle-Derived microRNAs in Metabolic Dysfunction-Associated Steatotic Liver Disease to Hepatocellular Carcinoma.Biomedicines · 2026Review
- MLKL in liver parenchymal cells promotes liver cancer in murine metabolic dysfunction-associated steatotic liver disease.Cell death & disease · 2026Article
- MicroRNA-21 promotes dysregulated lipid metabolism and hepatocellular carcinoma.Disease models & mechanisms · 2026Article
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
- The multifaceted roles of microRNAs in nonalcoholic steatohepatitis: from pathogenic mechanisms to diagnostic and therapeutic opportunities.Frontiers in genetics · 2026Review
- Machine Learning-Based Radiopatho-Clinical Model Integrating Ultrasound Radiomics and Kleiner Score for Prognosis Prediction in NAFLD-Related Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
- Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives.Journal of atherosclerosis and thrombosis · 2026Review
- Autophagy in the liver.Autophagy reports · 2026Review
- The Diagnostic Potential and Regulatory Mechanisms of miR-3180-3p in Metabolic Dysfunction-Associated Fatty Liver Disease with Respect to Inflammation and Oxidative Stress.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025Review
- Review
- Metabolic-Dysfunction-Associated Steatotic Liver Disease: Molecular Mechanisms, Clinical Implications, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Metabolomic Hallmarks of Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2024Review
Corrections and comments
- Update of
Authors and funding
17 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.