ArticleJournal of cellular and molecular medicine2020
AntagomiR-29b inhibits vascular and valvular calcification and improves heart function in rats.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Review
- Insights into preclinical models of calcific aortic valve disease and their translational potential.Frontiers in cardiovascular medicine · 2025Review
- Mechanisms of Cardiovascular Calcification and Experimental Models: Impact of Vitamin K Antagonists.Journal of clinical medicine · 2024Review
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- [miRNA-26a reduces vascular smooth muscle cell calcification by regulating connective tissue growth factor].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies.Reviews in cardiovascular medicine · 2022Review
- AntagomiR-29b inhibits vascular and valvular calcification and improves heart function in rats.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to investigate the role of the miR-29b and its effect on TGF-β3 pathway in vascular and valvular calcification in a rat model of calcific aortic valve diseases (CAVD). A rat model of CAVD was established by administration of warfarin plus vitamin K. The expression levels of miR-29b, osteogenic markers and other genes were determined by qRT-PCR, Western blot and/or immunofluorescence and immunohistochemistry. The calcium content and alkaline phosphatase (ALP) activity were measured. The calcium content, ALP activity and osteogenic markers levels in calcified aorta and aortic valve were augmented compared to controls. The expression of miR-29b, p-Smad3, and Wnt3 and β-catenin was significantly up-regulated, whereas TGF-β3 was markedly down-regulated. However, compared with the CAVD model group, the calcium content and ALP activity in rats treated with antagomiR-29b were significantly decreased, and antagomiR-29b administration reversed the effects of CAVD model on the expression of miR-29b and osteogenic markers. Inhibition of miR-29b in CAVD rats prevented from vascular and valvular calcification and induced TGF-β3 expression, suggesting that the miR-29b/TGF-β3 axis may play a regulatory role in the pathogenesis of vascular and valvular calcification and could play a significant role in the treatment of CAVD and other cardiovascular diseases.
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Registered trials
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