ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2016
Development of myotendinous-like junctions that anchor cardiac valves requires fibromodulin and lumican.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- A Proteomic Atlas of Human Milk: Uncovering Milk Functional Components.Research square · 2026Article
- Osteopontin-expressing valvular interstitial cell subpopulation as a driver of extracellular matrix remodeling in aortic valve disease.Frontiers in cardiovascular medicine · 2026Article
- Spatiotemporal gene expression and cellular dynamics of the developing human heart.Nature genetics · 2025Article
- Single-cell analysis reveals the loss of FABP4-positive proliferating valvular endothelial cells relates to functional mitral regurgitation.BMC medicine · 2024Article
- Temporal Progression of Aortic Valve Pathogenesis in a Mouse Model of Osteogenesis Imperfecta.Journal of cardiovascular development and disease · 2023Article
- Fibromodulin, a Multifunctional Matricellular Modulator.Journal of dental research · 2023Review
- Excess Provisional Extracellular Matrix: A Common Factor in Bicuspid Aortic Valve Formation.Journal of cardiovascular development and disease · 2021Review
- Lumican promotes joint fibrosis through TGF-β signaling.FEBS open bio · 2020Article
- Moderate Loss of the Extracellular Matrix Proteoglycan Lumican Attenuates Cardiac Fibrosis in Mice Subjected to Pressure Overload.Cardiology · 2020Article
- Investigating the role of super-enhancer RNAs underlying embryonic stem cell differentiation.BMC genomics · 2019Article
- The extracellular matrix proteoglycan lumican improves survival and counteracts cardiac dilatation and failure in mice subjected to pressure overload.Scientific reports · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThere are many patients that exhibit connective tissue related cardiac malformations but do not have mutations in collagen genes. The Small Leucine Rich Proteoglycans (SLRP) fibromodulin (FMOD) and lumican (LUM) bind collagen and regulate fibril assembly in other biological contexts.
resultsFMOD deficient mice and double deficient FMOD; LUM mice exhibited anomalies in regions where cardiac valve tissue interdigitates with adjacent muscle for support. Ectopic connective and/or myocardial tissue(s) was associated with the more severe cardiac valve anomalies in FMOD; LUM deficient mice. At postnatal day 0 (P0) there was an increase in the mesenchymal cell number in the regions where valve cusps anchor in FMOD; LUM deficient mice compared to WT. The cardiac valve anomalies correlated with the highest levels of FMOD expression in the heart and also where myotendinous junctions (MTJ) components biglycan, collagen type I alpha 1, and collagen type VI, are also localized.
conclusionsThe postnatal assembly of the collagen-rich ECM in regions where cardiac valves anchor, that we have designated 'myotendinous-like junctions' (MTLJ) requires the SLRPs FMOD and LUM. Moreover, FMOD and LUM may facilitate mesenchymal cell differentiation in late stages of cardiac valve development. Developmental Dynamics 245:1029-1042, 2016. © 2016 Wiley Periodicals, Inc.
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