ReviewFrontiers in cardiovascular medicine2022
Role of endothelial cells in vascular calcification.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Dietary index for gut microbiota score is inversely associated with carotid calcified plaque score in ischemic stroke patients.Frontiers in nutrition · 2026Article
- Integrative multivariate genomic analysis reveals shared genetic determinants and druggable targets for vascular calcification.Frontiers in medicine · 2026Article
- Endothelial adenosine receptor 2A loss alleviates diabetic vascular calcification by blocking CREB1-SNAI1-driven EndMT.Pharmacological research · 2025Article
- Article
- Article
- Role of abdominal aortic calcification score in predicting cardiovascular risk in the general population.Irish journal of medical science · 2025Article
- Unraveling the Mechanisms of Magnesium Supplementation in Alleviating Chronic Kidney Disease Complications and Progression: Balancing Risks and Benefits.Biological trace element research · 2025Review
- Role of miRNAs in Regulating Ascending Aortic Dilation in Bicuspid Aortic Valve Patients Operated for Aortic Stenosis.International journal of molecular sciences · 2025Article
- The relationship between programmed cell death and vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- A new SOFrontiers in physiology · 2025Article
- Exploring Bone Morphogenetic Protein-2 and -4 mRNA Expression and Their Receptor Assessment in a DynamicCells · 2024Article
- High Blood Pressure and Impaired Brain Health: Investigating the Neuroprotective Potential of Magnesium.International journal of molecular sciences · 2024Review
- Advances in regulating endothelial-mesenchymal transformation through exosomes.Stem cell research & therapy · 2024Review
- In Vitro Models of Cardiovascular Calcification.Biomedicines · 2024Review
- The predictive value of coronary artery calcium score combined with traditional risk factors for obstructive coronary heart disease in young people.BMC cardiovascular disorders · 2024Article
- Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.International journal of molecular sciences · 2024Review
- Smooth muscle cell-specific matrix metalloproteinase 3 deletion reduces osteogenic transformation and medial artery calcification.Cardiovascular research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification (VC) is active and regulates extraosseous ossification progress, which is an independent predictor of cardiovascular disease (CVD) morbidity and mortality. Endothelial cells (ECs) line the innermost layer of blood vessels and directly respond to changes in flow shear stress and blood composition. Together with vascular smooth muscle cells, ECs maintain vascular homeostasis. Increased evidence shows that ECs have irreplaceable roles in VC due to their high plasticity. Endothelial progenitor cells, oxidative stress, inflammation, autocrine and paracrine functions, mechanotransduction, endothelial-to-mesenchymal transition (EndMT), and other factors prompt ECs to participate in VC. EndMT is a dedifferentiation process by which ECs lose their cell lineage and acquire other cell lineages; this progress coexists in both embryonic development and CVD. EndMT is regulated by several signaling molecules and transcription factors and ultimately mediates VC
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What OpenQuestion holds
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.