ArticleJournal of biomechanics2012
Intracellular Ca(2+) accumulation is strain-dependent and correlates with apoptosis in aortic valve fibroblasts.
Article in Journal of biomechanics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- From biomechanical mechanisms to clinical reasoning: Deciphering mechanobiological drivers of aortic valve calcification for precision therapy.Mechanobiology in medicine · 2026Review
- In vitro model assesses the susceptibility of polymeric scaffolds for material-driven heart valve regeneration to calcification.In vitro models · 2025Article
- A Doppler-exclusive non-invasive computational diagnostic framework for personalized transcatheter aortic valve replacement.Scientific reports · 2023Article
- Mechanosensitive ion channels in apoptosis and ferroptosis: focusing on the role of Piezo1.BMB reports · 2023Review
- Intensive stretch-activated CRT-PMCA1 feedback loop promoted apoptosis of myoblasts through CaApoptosis : an international journal on programmed cell death · 2022Article
- Effect of iron overload on endothelial cell calcification and its mechanism.Annals of translational medicine · 2021Article
- Self-eating and Heart: The Emerging Roles of Autophagy in Calcific Aortic Valve Disease.Aging and disease · 2021Review
- On Valve Interstitial Cell Signaling: The Link Between Multiscale Mechanics and Mechanobiology.Cardiovascular engineering and technology · 2021Review
- High Pulsatile Load Decreases Arterial Stiffness: AnFrontiers in physiology · 2021Article
- A Fluid-Structure Interaction Study of Different Bicuspid Aortic Valve Phenotypes Throughout the Cardiac Cycle.Frontiers in physiology · 2021Article
- The effect of physiological stretch and the valvular endothelium on mitral valve proteomes.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- After 50 Years of Heart Transplants: What Does the Next 50 Years Hold for Cardiovascular Medicine? A Perspective From the International Society for Applied Cardiovascular Biology.Frontiers in cardiovascular medicine · 2019Article
- Valve Interstitial Cells: The Key to Understanding the Pathophysiology of Heart Valve Calcification.Journal of the American Heart Association · 2017Review
- Cell-matrix mechanics and pattern formation in inflammatory cardiovascular calcification.Heart (British Cardiac Society) · 2016Review
- Prediction of matrix-to-cell stress transfer in heart valve tissues.Journal of biological physics · 2015Article
- Impact of cellular microenvironment and mechanical perturbation on calcium signalling in meniscus fibrochondrocytes.European cells & materials · 2014Article
- Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I.Indian dermatology online journal · 2014Article
- Mechanisms of calcification in aortic valve disease: role of mechanokinetics and mechanodynamics.Current cardiology reports · 2013Review
- Effects of verapamil on the immediate-early gene expression of bone marrow mesenchymal stem cells stimulated by mechanical strain in vitro.Medical science monitor basic research · 2013Article
- Calcific nodule morphogenesis by heart valve interstitial cells is strain dependent.Biomechanics and modeling in mechanobiology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Aortic valve (AV) disease is often characterized by the formation of calcific nodules within AV leaflets that alter functional biomechanics. In vitro, formation of these nodules is associated with osteogenic differentiation and/or increased contraction and apoptosis of AV interstitial cells (AVICs), leading to growth of calcium phosphate crystal structures. In several other cell types, increased intracellular Ca(2+) has been shown to be an important part in activation of osteogenic differentiability. However, elevated intracellular Ca(2+) is known to mediate cell contraction, and has also been shown to lead to apoptosis in many cell types. Therefore, a rise in intracellular Ca(2+) may precede cellular changes that lead to calcification, and fibroblasts similar to AVICs have been shown to exhibit increases in intracellular Ca(2+) in response to mechanical strain. In this study, we hypothesized that strain induces intracellular Ca(2+) accumulation through stretch-activated calcium channels. We were also interested in assessing possible correlations between intracellular Ca(2+) increases and apoptosis in AVICs. To test our hypothesis, cultured porcine AVICs were used to assess correlates between strain, intracellular Ca(2+), and apoptosis. Ca(2+) sensitive fluorescent dyes were utilized to measure real-time intracellular Ca(2+) changes in strained AVICs. Ca(2+) changes were then correlated with AVIC apoptosis using flow cytometric Annexin V apoptosis assays. These data indicate that strain-dependent accumulation of intracellular Ca(2+) is correlated with apoptosis in AVICs. We believe that these findings indicate early mechanotransductive events that may initiate AV calcification pathways.
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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.