ArticleProceedings of the National Academy of Sciences of the United States of America2021
Loss of hepatic miR-33 improves metabolic homeostasis and liver function without altering body weight or atherosclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Context-dependent regulation of endothelial inflammation and atherosclerosis by endothelial microRNA-33.Atherosclerosis · 2026Article
- Non-coding RNAs in lipid metabolism and their roles in atherosclerosis.Nature reviews. Cardiology · 2026Review
- Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026Review
- Molecular Interplay between hypertension and dyslipidemia in cardiovascular pathogenesis: toward precision-based therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives.Journal of atherosclerosis and thrombosis · 2026Review
- The multifaceted roles of microRNAs in nonalcoholic steatohepatitis: from pathogenic mechanisms to diagnostic and therapeutic opportunities.Frontiers in genetics · 2026Review
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- The power of microRNA regulation-insights into immunity and metabolism.FEBS letters · 2025Review
- Exosomal non-coding RNAs: key regulators of inflammation-related cardiovascular disorders.European journal of medical research · 2025Review
- Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025Review
- Inhibiting MiR-33a-3p Expression Fails to Enhance ApoAI-Mediated Cholesterol Efflux in Pro-Inflammatory Endothelial Cells.Medicina (Kaunas, Lithuania) · 2025Article
- Exploring serum miR-33b as a novel diagnostic marker for hypercholesterolemia and obesity: insights from a pilot case-control study.BMC endocrine disorders · 2025Article
- miR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression.JCI insight · 2024Article
- Resveratrol suppresses hepatic fatty acid synthesis and increases fatty acid β-oxidation via the microRNA-33/SIRT6 signaling pathway.Experimental and therapeutic medicine · 2024Article
- Oligonucleotide therapies for nonalcoholic steatohepatitis.Molecular therapy. Nucleic acids · 2024Review
- microRNA-33 controls hunger signaling in hypothalamic AgRP neurons.Nature communications · 2024Article
- Time for micro-RNAs in steatotic liver disease: a case-control study.Frontiers in endocrinology · 2024Article
- Targeted Expression to Liver of an antimiR-33 Sponge as a Gene Therapy Strategy against Hypercholesterolemia: In Vitro Study.Current issues in molecular biology · 2023Article
- Inhibition of microRNA-33b in humanized mice ameliorates nonalcoholic steatohepatitis.Life science alliance · 2023Article
- Effects of miR-33 Deficiency on Metabolic and Cardiovascular Diseases: Implications for Therapeutic Intervention.International journal of molecular sciences · 2023Review
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
miR-33 is an intronic microRNA within the gene encoding the SREBP2 transcription factor. Like its host gene, miR-33 has been shown to be an important regulator of lipid metabolism. Inhibition of miR-33 has been shown to promote cholesterol efflux in macrophages by targeting the cholesterol transporter ABCA1, thus reducing atherosclerotic plaque burden. Inhibition of miR-33 has also been shown to improve high-density lipoprotein (HDL) biogenesis in the liver and increase circulating HDL-C levels in both rodents and nonhuman primates. However, evaluating the extent to which these changes in HDL metabolism contribute to atherogenesis has been hindered by the obesity and metabolic dysfunction observed in whole-body miR-33-knockout mice. To determine the impact of hepatic miR-33 deficiency on obesity, metabolic function, and atherosclerosis, we have generated a conditional knockout mouse model that lacks miR-33 only in the liver. Characterization of this model demonstrates that loss of miR-33 in the liver does not lead to increased body weight or adiposity. Hepatic miR-33 deficiency actually improves regulation of glucose homeostasis and impedes the development of fibrosis and inflammation. We further demonstrate that hepatic miR-33 deficiency increases circulating HDL-C levels and reverse cholesterol transport capacity in mice fed a chow diet, but these changes are not sufficient to reduce atherosclerotic plaque size under hyperlipidemic conditions. By elucidating the role of miR-33 in the liver and the impact of hepatic miR-33 deficiency on obesity and atherosclerosis, this work will help inform ongoing efforts to develop novel targeted therapies against cardiometabolic diseases.
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