ArticleJournal of the American Heart Association2017
Altered MicroRNA Expression Is Responsible for the Pro-Osteogenic Phenotype of Interstitial Cells in Calcified Human Aortic Valves.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Aortic Stenosis: Diagnosis, Molecular Mechanisms and Therapeutic Strategies-A Comprehensive Review.Journal of clinical medicine · 2025Review
- LncRNA NEAT1 sponges miR-214-3p to promote osteoblast differentiation through regulating the PI3K/AKT/mTOR pathway in aortic valve calcification.Scientific reports · 2025Article
- MicroRNA-143-3p and miR-452-5p: A Fingerprint for the Diagnosis of Aortic Stenosis in the Geriatric Population.Biomedicines · 2025Article
- 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
- Identification of hub genes and therapeutic drugs in osteonecrosis of the femoral head through integrated bioinformatics analysis and literature mining.Scientific reports · 2023Article
- MicroRNA-145 and microRNA-486 are potential serum biomarkers for vascular calcification.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- Network-Guided Multiomic Mapping of Aortic Valve Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- miR-486-5p expression is regulated by DNA methylation in osteosarcoma.BMC genomics · 2022Article
- The mechanistic pathways of oxidative stress in aortic stenosis and clinical implications.Theranostics · 2022Review
- Article
- MicroRNAs in Valvular Heart Diseases: Biological Regulators, Prognostic Markers and Therapeutical Targets.International journal of molecular sciences · 2021Review
- CircRNA TGFBR2/MiR-25-3p/TWIST1 axis regulates osteoblast differentiation of human aortic valve interstitial cells.Journal of bone and mineral metabolism · 2021Article
- Multi-Omics Approaches to Define Calcific Aortic Valve Disease Pathogenesis.Circulation research · 2021Review
- miR-214 Attenuates Aortic Valve Calcification by Regulating Osteogenic Differentiation of Valvular Interstitial Cells.Molecular therapy. Nucleic acids · 2020Article
- Article
- Aortic valve calcification in the era of non-coding RNAs: The revolution to come in aortic stenosis management?Non-coding RNA research · 2020Review
- The distribution of macrophage subtypes and their relationship to bone morphogenetic protein 2 in calcified aortic valve stenosis.American journal of translational research · 2020Article
- MicroRNA-204 Deficiency in Human Aortic Valves Elevates Valvular Osteogenic Activity.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe transition of aortic valve interstitial cells (AVICs) to myofibroblastic and osteoblast-like phenotypes plays a critical role in calcific aortic valve disease progression. Several microRNAs (miRs) are implicated in stem cell differentiation into osteoblast. We hypothesized that an epigenetic mechanism regulates valvular pro-osteogenic activity. This study examined miR profile in AVICs of calcified valves and identified miRs responsible for AVIC phenotypic transition. METHODS AND
resultsAVICs were isolated from normal and diseased valves. The miR microarray analysis revealed 14 upregulated and 12 downregulated miRs in diseased AVICs. Increased miR-486 and decreased miR-204 levels were associated with higher levels of myofibroblastic biomarker α-smooth muscle actin and osteoblastic biomarkers runt-related transcription factor 2 (Runx2) and osterix (Osx). Cotransfection of miR-486 antagomir and miR-204 mimic in diseased AVICs reduced their ability to express Runx2 and Osx. The miR-486 mimic upregulated α-smooth muscle actin expression in normal AVICs through the protein kinase B pathway and moderately elevated Runx2 and Osx levels. Knockdown of α-smooth muscle actin attenuated Runx2 and Osx expression induced by miR-486. The miR-486 mimic and miR-204 antagomir synergistically promoted Runx2 and Osx expression and calcium deposition in normal AVICs and normal aortic valve tissue.
conclusionsIn AVICs of calcified valves, increased levels of miR-486 induce myofibroblastic transition to upregulate Runx2 and Osx expression and synergize with miR-204 deficiency to elevate cellular and valvular pro-osteogenic activity. These novel findings indicate that modulation of the epigenetic mechanism underlying valvular pro-osteogenic activity has therapeutic potential for prevention of calcific aortic valve disease progression.
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