Aging-Associated miR-217 Aggravates Atherosclerosis and Promotes Cardiovascular Dysfunction.
Aging-Associated miR-217 Aggravates Atherosclerosis and Promotes Cardiovascular Dysfunction.
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DOI:
10.1161/atvbaha.120.314333
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发表时间:
2020-10
期刊:
影响因子:
--
通讯作者:
Ramiro AR
中科院分区:
文献类型:
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作者:
de Yébenes VG;Briones AM;Martos-Folgado I;Mur SM;Oller J;Bilal F;González-Amor M;Méndez-Barbero N;Silla-Castro JC;Were F;Jiménez-Borreguero LJ;Sánchez-Cabo F;Bueno H;Salaices M;Redondo JM;Ramiro AR
Supplemental Digital Content is available in the text. microRNAs are master regulators of gene expression with essential roles in virtually all biological processes. miR-217 has been associated with aging and cellular senescence, but its role in vascular disease is not understood. We have used an inducible endothelium-specific knock-in mouse model to address the role of miR-217 in vascular function and atherosclerosis. miR-217 reduced NO production and promoted endothelial dysfunction, increased blood pressure, and exacerbated atherosclerosis in proatherogenic apoE−/− mice. Moreover, increased endothelial miR-217 expression led to the development of coronary artery disease and altered left ventricular heart function, inducing diastolic and systolic dysfunction. Conversely, inhibition of endogenous vascular miR-217 in apoE−/− mice improved vascular contractility and diminished atherosclerosis. Transcriptome analysis revealed that miR-217 regulates an endothelial signaling hub and downregulates a network of eNOS (endothelial NO synthase) activators, including VEGF (vascular endothelial growth factor) and apelin receptor pathways, resulting in diminished eNOS expression. Further analysis revealed that human plasma miR-217 is a biomarker of vascular aging and cardiovascular risk. Our results highlight the therapeutic potential of miR-217 inhibitors in aging-related cardiovascular disease.