ArticleJournal of extracellular vesicles2025
Exomeres From Adventitial Fibroblasts of Spontaneously Hypertensive Rats Promote Vascular Remodelling via Transferring Osteopontin.
Article in Journal of extracellular vesicles, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Urolithin A alleviates vascular remodeling through mitochondrial SIRT3-mediated SOD2 deacetylation and antioxidation in hypertensive rats.Redox report : communications in free radical research · 2026Article
- Vascular adventitial cells and vascular remodeling: when a harp of thousand strings does not keep in tune so long.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Vascular adventitial fibroblasts (VAFs) contribute to vascular remodelling in hypertension. However, the mechanisms by which VAFs regulate vascular smooth muscle cells (VSMCs) in vascular remodelling are not well known. Here we report the crucial roles of extracellular nanoparticles exomeres (EMs) derived from VAFs in promoting VSMCs proliferation, migration and vascular remodelling in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). VSMCs' proliferation and migration were enhanced by EMs of SHR via the uptake of EMs in VSMCs, but not by EMs of WKY. Proteomics analysis showed that increased osteopontin (OPN) content may be responsible for the roles of EMs of SHR, which was confirmed by the fact that EMs of SHR pretreated with OPN knockdown lost their roles in promoting VSMCs proliferation and migration. OPN successively promoted the phosphorylation of FAK, PI3K and AKT via acting on integrin αVβ3. Inhibition of integrin αVβ3, FAK, PI3K or AKT almost abolished the effects of EMs of SHR on VSMCs proliferation and migration. Knockdown of OPN in the carotid artery attenuated local vascular remodelling in SHR. Repetitive intravenous injection of EMs of SHR increased blood pressure and promoted vascular remodelling in WKY and SHR. We conclude that EMs from VAFs of SHR promote VSMCs proliferation, migration and vascular remodelling via transferring OPN and subsequently activating integrin αVβ3/FAK/PI3K/AKT signalling pathway.
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Registered trials
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