ReviewClinical science (London, England : 1979)2017
In vitro 3D model and miRNA drug delivery to target calcific aortic valve disease.
Review in Clinical science (London, England : 1979), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Diverse functional roles of miR-128-3p in human diseases: Focus on its roles in human cancer.Genes & diseases · 2026Review
- Global burden of non-rheumatic calcific aortic valve disease in adults aged 60 years and older, with projections to 2041: insights from the Global Burden of Disease Study 2021.International journal of cardiology. Cardiovascular risk and prevention · 2026Article
- The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Deacetylated-poly-N-acetylglucosamine-folic Acid as a Nanocarrier for Delivering miR-196a Inhibitor to Anticancer Activity.Balkan medical journal · 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
- Telocytes-derived extracellular vesicles alleviate aortic valve calcification by carrying miR-30b.ESC heart failure · 2021Article
- Reproducible In Vitro Tissue Culture Model to Study Basic Mechanisms of Calcific Aortic Valve Disease: Comparative Analysis to Valvular Interstitials Cells.Biomedicines · 2021Article
- Adding a "Notch" to Cardiovascular Disease Therapeutics: A MicroRNA-Based Approach.Frontiers in cell and developmental biology · 2021Review
- Potential Roles of MyomiRs in Cardiac Development and Related Diseases.Current cardiology reviews · 2021Review
- Toward the Effective Bioengineering of a Pathological Tissue for Cardiovascular Disease Modeling: Old Strategies and New Frontiers for Prevention, Diagnosis, and Therapy.Frontiers in cardiovascular medicine · 2020Review
- Elastin-Dependent Aortic Heart Valve Leaflet Curvature Changes During Cyclic Flexure.Bioengineering (Basel, Switzerland) · 2019Article
- Engineering a 3D-Bioprinted Model of Human Heart Valve Disease Using Nanoindentation-Based Biomechanics.Nanomaterials (Basel, Switzerland) · 2018Article
- miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Drug Delivery and Nanoformulations for the Cardiovascular System.Research & reviews. Drug delivery · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Calcific aortic valve disease (CAVD) is the most prevalent valvular heart disease in the Western population, claiming 17000 deaths per year in the United States and affecting 25% of people older than 65 years of age. Contrary to traditional belief, CAVD is not a passive, degenerative disease but rather a dynamic disease, where initial cellular changes in the valve leaflets progress into fibrotic lesions that induce valve thickening and calcification. Advanced thickening and calcification impair valve function and lead to aortic stenosis (AS). Without intervention, progressive ventricular hypertrophy ensues, which ultimately results in heart failure and death. Currently, aortic valve replacement (AVR), surgical or transcatheter, is the only effective therapy to treat CAVD. However, these costly interventions are often delayed until the late stages of the disease. Nonetheless, 275000 are performed per year worldwide, and this is expected to triple by 2050. Given the current landscape, next-generation therapies for CAVD are needed to improve patient outcome and quality of life. Here, we first provide a background on the aortic valve (AV) and the pathobiology of CAVD as well as highlight current directions and future outlook on the development of functional 3D models of CAVD in vitro We then consider an often-overlooked aspect contributing to CAVD: miRNA (mis)regulation. Therapeutics could potentially normalize miRNA levels in the early stages of the disease and may slow its progression or even reverse calcification. We close with a discussion of strategies that would enable the use of miRNA as a therapeutic for CAVD. This focuses on an overview of controlled delivery technologies for nucleic acid therapeutics to the valve or other target tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.