ArticleArteriosclerosis, thrombosis, and vascular biology2023
Calciprotein Particles Induce Endothelial Dysfunction by Impairing Endothelial Nitric Oxide Metabolism.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Changes in vascular structure and function in primary hyperparathyroidism: a systematic review and meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Calciprotein particles disrupt autophagy in vascular endothelial cells and smooth muscle cells.Atherosclerosis plus · 2026Article
- Gla-Rich Protein (GRP): A Vitamin K-Dependent Regulator of Vascular Calcification, Inflammation, and Mineral Homeostasis.Current issues in molecular biology · 2026Review
- Stress hyperglycemia ratio and incident hypertension in chinese middle-aged and older adults: mediating roles of lipids in a prospective cohort.Lipids in health and disease · 2025Article
- The formation and function of calciprotein particles.Pflugers Archiv : European journal of physiology · 2025Review
- Mechanism of influence of calcified nanoparticles in the development of calcified diseases (Review).Biomedical reports · 2025Review
- Calciprotein particle-activated endothelial cells aggravate smooth muscle cell calcification via paracrine signalling.Cellular and molecular life sciences : CMLS · 2025Article
- [Advances in Animal Modeling in the Study of Bone-Vascular Axis Comorbidities].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
- Bidirectional crosstalk between the bone extracellular matrix and lysosomes in bone remodeling and osteoporosis.Frontiers in endocrinology · 2025Review
- Calciprotein particle counts associate with vascular remodelling in chronic kidney disease.Cardiovascular research · 2024Article
- The Bone-Vascular Axis: A Key Player in Chronic Kidney Disease Associated Vascular Calcification.Kidney diseases (Basel, Switzerland) · 2024Review
- Future of Uremic Toxin Management.Toxins · 2024Review
- Proteomic Profiling of Endothelial Cell Secretomes After Exposure to Calciprotein Particles Reveals Downregulation of Basement Membrane Assembly and Increased Release of Soluble CD59.International journal of molecular sciences · 2024Article
- Calciprotein particles induce arterial stiffening ex vivo and impair vascular cell function.Communications biology · 2024Article
- Review
- Review
- Serum Calcification Propensity T50 Is Associated with Soluble Thrombomodulin in Patients on Hemodialysis.Journal of clinical medicine · 2024Article
- Phosphate in Cardiovascular Disease: From New Insights Into Molecular Mechanisms to Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Magnesium and Vascular Calcification in Chronic Kidney Disease: Current Insights.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalciprotein particles (CPPs) are associated with the development of vascular calcifications in chronic kidney disease. The role of endothelial cells (ECs) in this process is unknown. Here, we investigated the interaction of CPPs and ECs, thereby focusing on endothelial nitric oxide metabolism and oxidative stress.
methodsCPPs were generated in calcium- and phosphate-enriched medium. Human umbilical vein endothelial cells were exposed to different concentrations of CPPs (0-100 µg/mL) for 24 or 72 hours. Ex vivo porcine coronary artery rings were used to measure endothelial cell-dependent vascular smooth muscle cell relaxation after CPP exposure. Serum samples from an early chronic kidney disease cohort (n=245) were analyzed for calcification propensity (measure for CPP formation) and nitrate and nitrite levels (NO
resultsCPP exposure for 24 hours reduced eNOS (endothelial nitric oxide synthase) mRNA expression and decreased nitrite production, indicating reduced nitric oxide bioavailability. Also, 24-hour CPP exposure caused increased mitochondria-derived superoxide generation, together with nitrotyrosine protein residue formation. Long-term (72 hours) exposure of human umbilical vein endothelial cells to CPPs induced eNOS uncoupling and decreased eNOS protein expression, indicating further impairment of the nitric oxide pathway. The ex vivo porcine coronary artery model showed a significant reduction in endothelial-dependent vascular smooth muscle cell relaxation after CPP exposure. A negative association was observed between NO
conclusionsCPPs cause endothelial cell dysfunction by impairing nitric oxide metabolism and generating oxidative stress. Our findings provide new evidence for direct effects of CPPs on ECs and pathways involved.
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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.