ArticleScientific reports2022
Endothelial-derived extracellular microRNA-92a promotes arterial stiffness by regulating phenotype changes of vascular smooth muscle cells.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.Electrolyte & blood pressure : E & BP · 2026Review
- Prognostic potential of circulatory miR-19a-3p, miR-19b-3p, and miR-329-3p for future hypertension diagnosis.Journal of hypertension · 2026Article
- MicroRNAs in Cardiovascular Diseases: Molecular Networks of Cellular Homeostasis, Inflammation, and Pathological Remodeling.International journal of molecular sciences · 2026Review
- Endothelin as a Treatment Target in Cardiovascular Diseases: A Recent Step Forward.Reviews in cardiovascular medicine · 2025Review
- Arterial stiffness and vascular aging: mechanisms, prevention, and therapy.Signal transduction and targeted therapy · 2025Review
- CircRNA-based AntimiR therapy: A novel approach to hypertension treatment.Non-coding RNA research · 2025Review
- miR-92a aggravates metabolic syndrome via KLF2/miR-483 axis.Journal of diabetes investigation · 2025Article
- Cardiovascular risk factors and modern therapeutic strategies in children and adolescents with type 1 diabetes to prevent future diabetic angiopathy in the era of innovative miRNAs biomarkers.Frontiers in endocrinology · 2025Review
- Epigenetic modifications in vascular inflammation.Frontiers in immunology · 2025Review
- The perspective of ceRNA regulation of circadian rhythm on choroidal neovascularization.Scientific reports · 2024Article
- Endothelial microRNAs in INOCA patients with diabetes mellitus.Cardiovascular diabetology · 2024Article
- Small RNA signatures of acute ischemic stroke in L1CAM positive extracellular vesicles.Scientific reports · 2024Article
- Ovariectomy-Induced Arterial Stiffening Differs From Vascular Aging and Is Reversed by GPER Activation.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- Extracellular Vesicles and Intercellular Communication: Challenges for In Vivo Molecular Imaging and Tracking.Pharmaceutics · 2023Review
- Lipid phosphate phosphatase 3 maintains NO-mediated flow-mediated dilatation in human adipose resistance arterioles.The Journal of physiology · 2023Article
- Extracellular Non-Coding RNAs in Cardiovascular Diseases.Pharmaceutics · 2023Review
- Paeonol Promotes Reendothelialization After Vascular Injury Through Activation of c-Myc/VEGFR2 Signaling Pathway.Drug design, development and therapy · 2023Article
- Emerging role of exosomes in vascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Epigenetic modifications as therapeutic targets in atherosclerosis: a focus on DNA methylation and non-coding RNAs.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Endothelial dysfunction and vascular smooth muscle cell (VSMC) plasticity are critically involved in the pathogenesis of hypertension and arterial stiffness. MicroRNAs can mediate the cellular communication between vascular endothelial cells (ECs) and neighboring cells. Here, we investigated the role of endothelial-derived extracellular microRNA-92a (miR-92a) in promoting arterial stiffness by regulating EC-VSMC communication. Serum miR-92a level was higher in hypertensive patients than controls. Circulating miR-92a level was positively correlated with pulse wave velocity (PWV), systolic blood pressure (SBP), diastolic blood pressure (DBP), and serum endothelin-1 (ET-1) level, but inversely with serum nitric oxide (NO) level. In vitro, angiotensin II (Ang II)-increased miR-92a level in ECs mediated a contractile-to-synthetic phenotype change of co-cultured VSMCs. In Ang II-infused mice, locked nucleic acid-modified antisense miR-92a (LNA-miR-92a) ameliorated PWV, SBP, DBP, and impaired vasodilation induced by Ang II. LNA-miR-92a administration also reversed the increased levels of proliferative genes and decreased levels of contractile genes induced by Ang II in mouse aortas. Circulating serum miR-92a level and PWV were correlated in these mice. These findings indicate that EC miR-92a may be transported to VSMCs via extracellular vesicles to regulate phenotype changes of VSMCs, leading to arterial stiffness.
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