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Published on: September 26, 2018
Aging-Associated miR-217 Aggravates Atherosclerosis and Promotes Cardiovascular Dysfunction
Virginia G de Yébenes1,2, Ana M Briones3,4, Inmaculada Martos-Folgado1
1Department of Vascular Physiopathology, B Lymphocyte Biology Lab (V.G.d.Y., I.M.-F., S.M.M., F.B., A.R.R.), Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
MicroRNA-217 (miR-217) drives vascular aging and atherosclerosis by reducing nitric oxide production. Inhibiting miR-217 shows therapeutic potential for cardiovascular disease.
Area of Science:
- Molecular Biology
- Cardiovascular Biology
- Aging Research
Background:
- MicroRNAs are key gene regulators in biological processes.
- miR-217 is linked to aging but its vascular disease role is unknown.
Purpose of the Study:
- Investigate miR-217's role in vascular function and atherosclerosis.
- Determine miR-217's potential as a biomarker for vascular aging.
Main Methods:
- Utilized an inducible endothelium-specific knock-in mouse model.
- Analyzed vascular function, blood pressure, and atherosclerosis development.
- Performed transcriptome analysis to identify miR-217 targets.
- Assessed human plasma miR-217 as a biomarker.
Main Results:
- Endothelial miR-217 overexpression impaired NO production, induced endothelial dysfunction, hypertension, and worsened atherosclerosis.
- miR-217 promoted coronary artery disease and cardiac dysfunction.
- Inhibiting miR-217 improved vascular function and reduced atherosclerosis.
- miR-217 downregulates eNOS activators (VEGF, apelin receptor pathways).
- Plasma miR-217 correlates with vascular aging and cardiovascular risk.
Conclusions:
- miR-217 is a critical regulator of vascular aging and atherosclerosis.
- Inhibiting miR-217 offers a potential therapeutic strategy for cardiovascular disease.
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