ArticleScientific reports2025
Icariin inhibits proliferation and migration of VSMCs via LncRNA H19 competitively binding to HuR.
Article in Scientific reports, 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Review
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Developing new anti-atherosclerotic agents and exploring their mechanistic actions is required. This study defined the molecular mechanism of icariin (ICA) in human aortic smooth muscle cells (HA-VSMCs) proliferation and migration by focusing on lncRNA H19 mediated the ability of the HuR protein to bind target mRNAs. The levels of lncRNA H19, cyclin D1 and matrix metalloproteinase-9 (MMP-9) were measured via qPCR or western blot. The 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium (MTS), flow cytometry and transwell assays were performed to determine the functions of lncRNA H19 in cell proliferation and migration. RNA pull down and RIP were performed to verify the interaction between lncRNA H19 and HuR, or interaction between HuR and target mRNAs. LncRNA H19 expression was modulated in response to treatment with ICA. LncRNA H19 overexpression inhibited the proliferation and migration of ox-LDL-induced HA-VSMCs. ICA attenuated cell proliferation and migration, which was reversed by lncRNA H19 knockdown. LncRNA H19 overexpression reduced the expression of cyclin D1/MMP-9, and restrained the stability of cyclin D1/MMP-9 mRNAs. Moreover, lncRNA H19 was found to bind with HuR to decrease the mRNA stability of cyclin D1/MMP-9 mRNAs. In addition, ICA suppressed the expression of cyclin D1/MMP-9, this effect was partly reversed by lncRNA H19 knockdown. We propose that lncRNA H19 serves as an endogenous competing RNA to disable HuR, restricting its availability to target cyclin D1/MMP-9 mRNAs, generally repressing HA-VSMCs proliferation and migration. ICA inhibits proliferation and migration of HA-VSMCs, altering the expression of cyclin D1 and MMP-9, in a lncRNA H19/HuR dependent manner.
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