ArticleCirculation research2014
Control of very low-density lipoprotein secretion by N-ethylmaleimide-sensitive factor and miR-33.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Noncoding RNAs as additional mediators of epigenetic regulation in nonalcoholic fatty liver disease.World journal of gastroenterology · 2022Review
- MicroRNA regulation of cholesterol metabolism.Annals of the New York Academy of Sciences · 2021Review
- Loss of hepatic miR-33 improves metabolic homeostasis and liver function without altering body weight or atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Promises of Nanotherapeutics in Obesity.Trends in endocrinology and metabolism: TEM · 2019Review
- Non-coding RNAs in lipid metabolism.Vascular pharmacology · 2019Review
- Posttranscriptional regulation of lipid metabolism by non-coding RNAs and RNA binding proteins.Seminars in cell & developmental biology · 2018Review
- Genetic Ablation of miR-33 Increases Food Intake, Enhances Adipose Tissue Expansion, and Promotes Obesity and Insulin Resistance.Cell reports · 2018Article
- Genetic Dissection of the Impact of miR-33a and miR-33b during the Progression of Atherosclerosis.Cell reports · 2017Article
- MicroRNAs and lipid metabolism.Current opinion in lipidology · 2017Review
- Structure, Function and Metabolism of Hepatic and Adipose Tissue Lipid Droplets: Implications in Alcoholic Liver Disease.Current molecular pharmacology · 2017Review
- miRNA regulation of LDL-cholesterol metabolism.Biochimica et biophysica acta · 2016Review
- miRNAs and High-Density Lipoprotein metabolism.Biochimica et biophysica acta · 2016Review
- Truths and controversies concerning the role of miRNAs in atherosclerosis and lipid metabolism.Current opinion in lipidology · 2016Review
- Liver microRNAs: potential mediators and biomarkers for metabolic and cardiovascular disease?European heart journal · 2016Review
- Nanomedicine Meets microRNA: Current Advances in RNA-Based Nanotherapies for Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- Micro-RNAs and High-Density Lipoprotein Metabolism.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- microRNAs in lipoprotein metabolism and cardiometabolic disorders.Atherosclerosis · 2016Review
- miR-27b inhibits LDLR and ABCA1 expression but does not influence plasma and hepatic lipid levels in mice.Atherosclerosis · 2015Article
- Role of microRNAs in Alcohol-Induced Multi-Organ Injury.Biomolecules · 2015Review
- MicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels.Nature medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleSeveral reports suggest that antisense oligonucleotides against miR-33 might reduce cardiovascular risk in patients by accelerating the reverse cholesterol transport pathway. However, conflicting reports exist about the impact of anti-miR-33 therapy on the levels of very low-density lipoprotein-triglycerides (VLDL-TAG).
objectiveWe test the hypothesis that miR-33 controls hepatic VLDL-TAG secretion. METHODS AND
resultsUsing therapeutic silencing of miR-33 and adenoviral overexpression of miR-33, we show that miR-33 limits hepatic secretion of VLDL-TAG by targeting N-ethylmaleimide-sensitive factor (NSF), both in vivo and in primary hepatocytes. We identify conserved sequences in the 3'UTR of NSF as miR-33 responsive elements and show that Nsf is specifically recruited to the RNA-induced silencing complex following induction of miR-33. In pulse-chase experiments, either miR-33 overexpression or knock-down of Nsf lead to decreased secretion of apolipoproteins and TAG in primary hepatocytes, compared with control cells. Importantly, Nsf rescues miR-33-dependent reduced secretion. Finally, we show that overexpression of Nsf in vivo increases global hepatic secretion and raises plasma VLDL-TAG.
conclusionsTogether, our data reveal key roles for the miR-33-NSF axis during hepatic secretion and suggest that caution should be taken with anti-miR-33-based therapies because they might raise proatherogenic VLDL-TAG levels.
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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 OpenQuestion graph.