ArticleBiomaterials2017
Myofibroblastic activation of valvular interstitial cells is modulated by spatial variations in matrix elasticity and its organization.
Article in Biomaterials, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 108 citations in OpenAlex.
- From biomechanical mechanisms to clinical reasoning: Deciphering mechanobiological drivers of aortic valve calcification for precision therapy.Mechanobiology in medicine · 2026Review
- Sex-Specific Remodeling Phenotypes of the Tricuspid Valve Leaflets in an Ovine Model of Functional Tricuspid Regurgitation.bioRxiv : the preprint server for biology · 2026Article
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- 3D chemotaxis chip for investigating natural killer cell migration mechanisms.Frontiers in immunology · 2026Article
- Trimethylamine-N-oxide promotes fibrotic activation of quiescent valvular interstitial cells via endoplasmic reticulum stress.Scientific reports · 2025Article
- Reversion of aortic valve cells calcification by activation of Notch signalling via histone acetylation induction.Signal transduction and targeted therapy · 2025Article
- Tricuspid valve leaflet remodeling in sheep with biventricular heart failure: A comparison between leaflets.Acta biomaterialia · 2025Article
- Trpv4-mediated mechanotransduction regulates the differentiation of valvular interstitial cells to myofibroblasts: implications for aortic valve stenosis.American journal of physiology. Cell physiology · 2025Article
- Transient Receptor Potential Vanilloid 4 Calcium-Permeable Channel Contributes to Valve Stiffening in Aortic Stenosis.Journal of the American Heart Association · 2025Article
- Photoresponsive Chemistries for User-Directed Hydrogel Network Modulation to Investigate Cell-Matrix Interactions.Accounts of chemical research · 2025Review
- Unraveling the Mechanisms of Valvular Heart Disease to Identify Medical Therapy Targets: A Scientific Statement From the American Heart Association.Circulation · 2024Review
- Non-immune factors cause prolonged myofibroblast phenotype in implanted synthetic heart valve scaffolds.Applied materials today · 2024Article
- Melt-electrowriting-enabled anisotropic scaffolds loaded with valve interstitial cells for heart valve tissue Engineering.Journal of nanobiotechnology · 2024Article
- Dynamic reporters for probing real-time activation of human fibroblasts from single cells to populations.APL bioengineering · 2024Article
- Intracellular proteomics and extracellular vesiculomics as a metric of disease recapitulation in 3D-bioprinted aortic valve arrays.Science advances · 2024Article
- Incidence of systemic inflammatory response syndrome and patient outcome following transcatheter edge-to-edge mitral valve repair.Clinical research in cardiology : official journal of the German Cardiac Society · 2024Article
- Nanocellulose-based porous materials: Regulation and pathway to commercialization in regenerative medicine.Bioactive materials · 2023Review
- Exploring molecular profiles of calcification in aortic vascular smooth muscle cells and aortic valvular interstitial cells.Journal of molecular and cellular cardiology · 2023Article
- Construction of cardiac fibrosis for biomedical research.Smart medicine · 2023Review
- Activation of Piezo1 promotes osteogenic differentiation of aortic valve interstitial cell through YAP-dependent glutaminolysis.Science advances · 2023Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Valvular interstitial cells (VICs) are key regulators of the heart valve's extracellular matrix (ECM), and upon tissue damage, quiescent VIC fibroblasts become activated to myofibroblasts. As the behavior of VICs during disease progression and wound healing is different compared to healthy tissue, we hypothesized that the organization of the matrix mechanics, which results from depositing of collagen fibers, would affect VIC phenotypic transition. Specifically, we investigated how the subcellular organization of ECM mechanical properties affects subcellular localization of Yes-associated protein (YAP), an early marker of mechanotransduction, and α-smooth muscle actin (α-SMA), a myofibroblast marker, in VICs. Photo-tunable hydrogels were used to generate substrates with different moduli and to create organized and disorganized patterns of varying elastic moduli. When porcine VICs were cultured on these matrices, YAP and α-SMA activation were significantly increased on substrates with higher elastic modulus or a higher percentage of stiff regions. Moreover, VICs cultured on substrates with a spatially disorganized elasticity had smaller focal adhesions, less nuclear localized YAP, less α-SMA organization into stress fibers and higher proliferation compared to those cultured on substrates with a regular mechanical organization. Collectively, these results suggest that disorganized spatial variations in mechanics that appear during wound healing and fibrotic disease progression may influence the maintenance of the VIC fibroblast phenotype, causing more proliferation, ECM remodeling and matrix deposition.
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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.