ArticleJournal of extracellular vesicles2020
MiR155-5p in adventitial fibroblasts-derived extracellular vesicles inhibits vascular smooth muscle cell proliferation via suppressing angiotensin-converting enzyme expression.
Article in Journal of extracellular vesicles, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 113 citations in OpenAlex.
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- MicroRNAs and SGLT2 inhibitors in cardiovascular disease: Shared pathways and emerging roles.Journal of molecular and cellular cardiology plus · 2026Review
- Neoagarotetraose from Marine Red Algae Attenuates Hypertensive Vascular Remodeling by Targeting FoxO4 to Inhibit Mitochondrial Superoxide Generation.Journal of agricultural and food chemistry · 2026Article
- The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.Electrolyte & blood pressure : E & BP · 2026Review
- Bacterial Extracellular Vesicles Mediate Microbiota-Host Communication to Regulate Blood Pressure in Male Rats.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Role of Extracellular Vesicles in Abdominal Aortic Aneurysm: Pathophysiology, Biomarkers, and Therapeutic Potentials.International journal of molecular sciences · 2026Review
- Vascular adventitial cells and vascular remodeling: when a harp of thousand strings does not keep in tune so long.Frontiers in physiology · 2026Review
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Exosomes in hypertension: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.Redox report : communications in free radical research · 2025Article
- Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025Review
- The emerging role of Nrf2 in heart failure: From cardioprotection to therapeutic approaches.ESC heart failure · 2025Review
- Identification of miRNA biomarkers for essential hypertension in small samples based on MPGAM.Scientific reports · 2025Article
- Progress in exosome-related research supported by the National Natural Science Foundation of China.Fundamental research · 2025Review
- Exomeres From Adventitial Fibroblasts of Spontaneously Hypertensive Rats Promote Vascular Remodelling via Transferring Osteopontin.Journal of extracellular vesicles · 2025Article
- Involvement of miRNAs in the Cluster of Metabolic Factors of MetS: Nutrition-Genome-MetS Axis.Journal of clinical medicine · 2025Review
- Role of Exosomes in Cardiovascular Disease: A Key Regulator of Intercellular Communication in Cardiomyocytes.ACS omega · 2025Review
- Sodium pump subunit NKAα1 protects against diabetic endothelial dysfunction by inhibiting ferroptosis through the autophagy-lysosome degradation of ACSL4.Clinical and translational medicine · 2025Article
- Single-cell RNA sequencing of the carotid artery and femoral artery of rats exposed to hindlimb unloading.Cellular and molecular life sciences : CMLS · 2025Article
- Identification of an Exosomal miRNA Signature in Newly Diagnosed Essential Hypertensive Adults.British journal of biomedical science · 2025Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proliferation of vascular smooth muscle cells (VSMCs) plays crucial roles in vascular remodelling and stiffening in hypertension. Vascular adventitial fibroblasts are a key regulator of vascular wall function and structure. This study is designed to investigate the roles of adventitial fibroblasts-derived extracellular vesicles (EVs) in VSMC proliferation and vascular remodelling in normotensive Wistar-Kyoto rat (WKY) and spontaneously hypertensive rat (SHR), an animal model of human essential hypertension. EVs were isolated from aortic adventitial fibroblasts of WKY (WKY-EVs) and SHR (SHR-EVs). Compared with WKY-EVs, miR155-5p content was reduced, while angiotensin-converting enzyme (ACE) content was increased in SHR-EVs. WKY-EVs inhibited VSMC proliferation of SHR, which was prevented by miR155-5p inhibitor. SHR-EVs promoted VSMC proliferation of both strains, which was enhanced by miR155-5p inhibitor, but abolished by captopril or losartan. Dual luciferase reporter assay showed that ACE was a target gene of miR155-5p. MiR155-5p mimic or overexpression inhibited VSMC proliferation and ACE upregulation of SHR. WKY-EVs reduced ACE mRNA and protein expressions while SHR-EVs only increased ACE protein level in VSMCs of both strains. However, the SHR-EVs-derived from the ACE knockdown-treated adventitial fibroblasts lost the roles in promoting VSMC proliferation and ACE upregulation. Systemic miR155-5p overexpression reduced vascular ACE, angiotensin II and proliferating cell nuclear antigen levels, and attenuated hypertension and vascular remodelling in SHR. Repetitive intravenous injection of SHR-EVs increased blood pressure and vascular ACE contents, and promoted vascular remodelling in both strains, while WKY-EVs reduced vascular ACE contents and attenuated hypertension and vascular remodelling in SHR. We concluded that WKY-EVs-mediated miR155-5p transfer attenuates VSMC proliferation and vascular remodelling in SHR via suppressing ACE expression, while SHR-EVs-mediated ACE transfer promotes VSMC proliferation and vascular remodelling.
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