ArticleCirculation research2010
Reduced sox9 function promotes heart valve calcification phenotypes in vivo.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Anatomy, Histology, Aetiology, Development and Functions of Cartilago Cordis: A Systematic Review.Cells, tissues, organs · 2025Pooled it
- Regulation of human chondrocyte function through direct inhibition of cartilage master regulator SOX9 by microRNA-145 (miRNA-145).The Journal of biological chemistry · 2012Trial
- A loss-of-function polymorphism in the propeptide of lysyl oxidase exacerbates atherosclerosis.JCI insight · 2026Article
- Knockdown of ARID1A Protects H9c2 Cells Against Hypoxia/Reoxygenation (H/R)-Induced Injury by Targeting SOX9.Korean circulation journal · 2026Article
- The intersection of disorders of sex development and cardiovascular diseases.Biology of sex differences · 2026Review
- Role of SOX9 in cardiovascular diseases: Evidence today.World journal of cardiology · 2025Review
- Profibrotic role of the SOX9-MMP10-ECM biosynthesis axis in the tracheal fibrosis after injury and repair.Genes & diseases · 2024Article
- Significance of Fibrillin-1, Filamin A, MMP2 and SOX9 in Mitral Valve Pathology.International journal of molecular sciences · 2024Article
- Role of AOX1 on RXR signaling regulates osteoblastogenesis in hPDLMSCs.Scientific reports · 2024Article
- Cell diversity and plasticity during atrioventricular heart valve EMTs.Nature communications · 2023Article
- Inhibition of miR-101-3p prevents human aortic valve interstitial cell calcification through regulation of CDH11/SOX9 expression.Molecular medicine (Cambridge, Mass.) · 2023Article
- Angiopoietin-like 2 is essential to aortic valve development in mice.Communications biology · 2022Article
- Monocytes and pyrophosphate promote mesenchymal stem cell viability and early osteogenic differentiation.Journal of materials science. Materials in medicine · 2022Article
- Increased TGFβ1 and SMAD3 Contribute to Age-Related Aortic Valve Calcification.Frontiers in cardiovascular medicine · 2022Article
- Sex-Differences in Aortic Stenosis: Mechanistic Insights and Clinical Implications.Frontiers in cardiovascular medicine · 2022Article
- Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Spontaneous Degenerative Aortic Valve Disease in New Zealand Obese Mice.Journal of the American Heart Association · 2021Article
- Comparison of Serotonin-Regulated Calcific Processes in Aortic and Mitral Valvular Interstitial Cells.ACS omega · 2021Article
- Roles of Nuclear Receptors in Vascular Calcification.International journal of molecular sciences · 2021Review
- Diabetes Mellitus and Its Implications in Aortic Stenosis Patients.International journal of molecular sciences · 2021Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleCalcification of heart valve structures is the most common form of valvular disease and is characterized by the appearance of bone-like phenotypes within affected structures. Despite the clinical significance, the underlying etiology of disease onset and progression is largely unknown and valve replacement remains the most effective treatment. The SRY-related transcription factor Sox9 is expressed in developing and mature heart valves, and its function is required for expression of cartilage-associated proteins, similar to its role in chondrogenesis. In addition to cartilage-associated defects, mice with reduced sox9 function develop skeletal bone prematurely; however, the ability of sox9 deficiency to promote ectopic osteogenic phenotypes in heart valves has not been examined.
objectiveThis study aims to determine the role of Sox9 in maintaining connective tissue homeostasis in mature heart valves using in vivo and in vitro approaches. METHODS AND
resultsUsing histological and molecular analyses, we report that, from 3 months of age, Sox9(fl/+);Col2a1-cre mice develop calcific lesions in heart valve leaflets associated with increased expression of bone-related genes and activation of inflammation and matrix remodeling processes. Consistently, ectopic calcification is also observed following direct knockdown of Sox9 in heart valves in vitro. Furthermore, we show that retinoic acid treatment in mature heart valves is sufficient to promote calcific processes in vitro, which can be attenuated by Sox9 overexpression.
conclusionsThis study provides insight into the molecular mechanisms of heart valve calcification and identifies reduced Sox9 function as a potential genetic basis for calcific valvular disease.
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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.