ArticleAmerican journal of physiology. Cell physiology2012
A dynamic model of calcific nodule destabilization in response to monocyte- and oxidized lipid-induced matrix metalloproteinases.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Discovery, Characterization, and Anti-XOD Activity of Calcium Metallophore fromOrganic letters · 2025Article
- The interplay of collagen, macrophages, and microcalcification in atherosclerotic plaque cap rupture mechanics.Basic research in cardiology · 2024Review
- History of fragility fracture is associated with cardiovascular mortality in hemodialysis patients: the Q-Cohort study.Journal of bone and mineral metabolism · 2024Article
- Mechanism Analysis of Vascular Calcification Based on Fluid Dynamics.Diagnostics (Basel, Switzerland) · 2023Review
- Exosomes and Atherogenesis.Frontiers in cardiovascular medicine · 2021Review
- The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification.Frontiers in cardiovascular medicine · 2021Review
- Bone mineral density and mortality in end-stage renal disease patients.Clinical kidney journal · 2020Review
- It takes more than two to tango: mechanosignaling of the endothelial surface.Pflugers Archiv : European journal of physiology · 2020Review
- Review
- COMP-lex Mechanics: Matricrine Signaling.Circulation research · 2016Article
- Blood flow modulation of vascular dynamics.Current opinion in lipidology · 2015Review
- Stretchable electrochemical impedance sensors for intravascular detection of lipid-rich lesions in New Zealand White rabbits.Biosensors & bioelectronics · 2014Article
- Macrophage-derived matrix vesicles: an alternative novel mechanism for microcalcification in atherosclerotic plaques.Circulation research · 2013Article
- Elevated electrochemical impedance in the endoluminal regions with high shear stress: implication for assessing lipid-rich atherosclerotic lesions.Biosensors & bioelectronics · 2013Article
- Visualizing novel concepts of cardiovascular calcification.Trends in cardiovascular medicine · 2013Review
- Atmospheric ultrafine particles promote vascular calcification via the NF-κB signaling pathway.American journal of physiology. Cell physiology · 2013Article
- Mechanisms and clinical consequences of vascular calcification.Frontiers in endocrinology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Vulnerable plaque remains clinically undetectable, and there is no accepted in vitro model. We characterize the calcific nodules produced by calcifying vascular cells (CVC) in ApoE-null mice, demonstrating increased destabilization of cultured nodules in the presence of oxidized low-density lipoprotein (oxLDL) and monocytes under pulsatile shear stress. CVC implanted in the subcutaneous space of hyperlipidemic mice produced nodules revealing features of calcific atherosclerotic plaque including a fibrous cap, cholesterol clefts, thin shoulder, lipids, and calcium mineral deposits. CVC nodules seeded in the pulsatile flow channel (τ(avg) = 23 dyn/cm(2), ∂τ/∂t = 71 dyn·cm(-2)·s(-1)) underwent deformation and destabilization. Computational fluid dynamics revealed distinct shear force profiles on the nodules. Presence of oxLDL or monocytic THP-1 cells significantly increased the numbers of nodules destabilized from the substrate. Both oxLDL and THP-1 increased matrix metalloproteinase (MMP) activity in CVC. The MMP inhibitor GM6001 significantly reversed oxLDL- and THP-1-induced nodule destabilization, whereas overexpression of MMP-9 increased destabilization. These findings demonstrate that CVC-derived nodules resembled calcific atherosclerotic plaque and were destabilized in the presence of active lipids and monocytes via induction of MMPs.
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