ArticleInternational journal of molecular sciences2019
MicroRNA-204 Deficiency in Human Aortic Valves Elevates Valvular Osteogenic Activity.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Shared pathophysiological mechanisms between diabetes and calcific aortic valve disease: an immunometabolic perspective.Cardiovascular diabetology · 2026Review
- The Heart's Small Molecules: The Importance of MicroRNAs in Cardiovascular Health.Journal of clinical medicine · 2025Review
- Aortic Stenosis: Diagnosis, Molecular Mechanisms and Therapeutic Strategies-A Comprehensive Review.Journal of clinical medicine · 2025Review
- Involvement of miRNA-204 carried by the exosomes of macrophages in the AT2 receptor-mediated improvement of vascular calcification.Cellular and molecular life sciences : CMLS · 2025Article
- MicroRNA-143-3p and miR-452-5p: A Fingerprint for the Diagnosis of Aortic Stenosis in the Geriatric Population.Biomedicines · 2025Article
- The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Noncoding RNA regulates the expression of Krm1 and Dkk2 to synergistically affect aortic valve lesions.Experimental & molecular medicine · 2024Article
- Cathepsin D elevates the fibrocalcific activity in human aortic valve cells through the ERK1/2-Sox9 pathway.Frontiers in cardiovascular medicine · 2024Article
- The Role of MicroRNAs in Aortic Stenosis-Lessons from Recent Clinical Research Studies.International journal of molecular sciences · 2023Review
- miR-199a-5p inhibits aortic valve calcification by targeting ATF6 and GRP78 in valve interstitial cells.Open medicine (Warsaw, Poland) · 2023Article
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- Interleukin 38 alleviates aortic valve calcification by inhibition of NLRP3.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity.Molecular medicine (Cambridge, Mass.) · 2022Article
- The microRNA-204-5p inhibits APJ signalling and confers resistance to cardiac hypertrophy and dysfunction.Clinical and translational medicine · 2022Article
- CircRNA TGFBR2/MiR-25-3p/TWIST1 axis regulates osteoblast differentiation of human aortic valve interstitial cells.Journal of bone and mineral metabolism · 2021Article
- MicroRNAs Modulate Signaling Pathways in Osteogenic Differentiation of Mesenchymal Stem Cells.International journal of molecular sciences · 2021Review
- NcRNAs in Vascular and Valvular Intercellular Communication.Frontiers in molecular biosciences · 2021Review
- miRNA Expression Profiling Uncovers a Role of miR-139-5p in Regulating the Calcification of Human Aortic Valve Interstitial Cells.Frontiers in genetics · 2021Article
- Monocytes enhance the inflammatory response to TLR2 stimulation in aortic valve interstitial cells through paracrine up-regulation of TLR2 level.International journal of biological sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aortic valve interstitial cells (AVICs) play a major role in valvular calcification associated with calcific aortic valve disease (CAVD). Although AVICs from diseased valves display a pro-osteogenic phenotype, the underlying mechanism causing this remains unclear. MicroRNA-204 (miR-204) is a negative regulator of osteoblast differentiation. We sought to analyze miR-204 expression in diseased human aortic valves and determine the role of this miR in AVIC osteogenic activity associated with CAVD pathobiology. In situ hybridization and PCR analysis revealed miR-204 deficiency in diseased valves and in AVICs from diseased valves. MiR-204 mimic suppressed alkaline phosphatase (ALP) expression and calcium deposition in AVICs from diseased valves. MiR-204 antagomir enhanced ALP expression in AVICs from normal valves through induction of Runx2 and Osx, and expression of miR-204 antagomir in mouse aortic valves promoted calcium deposition through up-regulation of Runx2 and Osx. Further, miR-204 mimic suppressed the osteogenic responses to TGF-β1 in AVICs of normal valves. In conclusion, miR-204 deficiency contributes to the mechanism underlying elevated osteogenic activity in diseased aortic valves, and miR-204 is capable of reversing the pro-osteogenic phenotype of AVICs of diseased valves and suppressing AVIC osteogenic response to stimulation. Exogenous miR-204 may have therapeutic potential for inhibiting valvular calcification associated with CAVD progression.
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