ArticleiScience2020
A Key GWAS-Identified Genetic Variant Contributes to Hyperlipidemia by Upregulating miR-320a.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Specific circulating miRNAs are associated with plasma lipids in a healthy American cohort.Physiological genomics · 2024Article
- miR-320a induces pancreatic β cells dysfunction in diabetes by inhibiting MafF.Molecular therapy. Nucleic acids · 2021Article
- Genetic Variants in Transcription Factor Binding Sites in Humans: Triggered by Natural Selection and Triggers of Diseases.International journal of molecular sciences · 2021Review
- Roles of MicroRNAs in Glucose and Lipid Metabolism in the Heart.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been unclear whether the elevated levels of the circulating miR-320a in patients with coronary artery disease is due to environmental influence or genetic basis. By recombinant adeno-associated virus (rAAV)-mediated loss- and gain-of-function studies in the mouse liver, we revealed that elevated miR-320a is sufficient to aggravate diet-induced hyperlipidemia and hepatic steatosis. Then, we analyzed the data from published genome-wide association studies and identified the rs12541335 associated with hyperlipidemia. We demonstrated that the rs13282783 T allele indeed obligated the silencer activity by preventing the repressor ZFP161 and co-repressor HDAC2 from binding to DNA that led to miR-320a upregulation. We further confirmed this genetic connection on an independent population and through direct genome editing in liver cells. Besides environmental (diet) influence, we established a genetic component in the regulation of miR-320a expression, which suggest a potential therapeutic avenue to treat coronary artery disease by blocking miR-320a in patient liver.
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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.