ReviewJournal of atherosclerosis and thrombosis2021
Phosphate as a Pathogen of Arteriosclerosis and Aging.
Review in Journal of atherosclerosis and thrombosis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 68 citations in OpenAlex.
- Phosphate homeostasis and apparent treatment-resistant hypertension in chronic kidney disease: the Chronic Renal Insufficiency Cohort (CRIC) study.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- TMEM174 Deficiency Reduces Longevity by Promoting Phosphate-Driven Vascular Calcification.Research square · 2026Article
- Inverse Association between T50 Calciprotein Crystallization (Serum Calcification Propensity) and Carotid Artery Intima-Media Thickness in Health Examinees with a Reduced Kidney Function.Journal of atherosclerosis and thrombosis · 2026Article
- Association between admission serum phosphate levels and prognosis in post-cardiac arrest patients: a retrospective observational study.BMC cardiovascular disorders · 2026Observational
- TMEM174 Deficiency Reduces Longevity by Promoting Phosphate-Driven Vascular Calcification.bioRxiv : the preprint server for biology · 2026Article
- Overview of the Zinc Functional Interactome Through Health Hallmarks and Medical Conditions.Nutrients · 2026Review
- Estimated T50 calciprotein crystallization test in patients undergoing hemodialysis: Osaka Dialysis Complication Study (ODCS).Clinical and experimental nephrology · 2025Observational
- Zinc Deficiency in Chronic Kidney Disease and Hemodialysis: Insights from Basic Research to Clinical Implications.Nutrients · 2025Review
- ApoE [-/-] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages.Atherosclerosis plus · 2025Article
- T50 Calciprotein Crystallization and the Decreased Role of Fetuin-A in Type 2 Diabetes.Journal of atherosclerosis and thrombosis · 2025Article
- Inflammasome Activation and Neutrophil Extracellular Traps in Atherosclerosis.Journal of atherosclerosis and thrombosis · 2025Review
- Article
- Mineral Stress Drives Loss of Heterochromatin: An Early Harbinger of Vascular Inflammaging and Calcification.Circulation research · 2025Article
- Molecular mechanisms and therapeutic progress in atherosclerosis: bridging immune inflammation and precision medicine.Frontiers in immunology · 2025Review
- Phosphate overload via the type III Na-dependent Pi transporter represses aortic wall elastic fiber formation.Fujita medical journal · 2024Article
- Article
- Phosphate in Cardiovascular Disease: From New Insights Into Molecular Mechanisms to Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Correlation between serum phosphate and all-cause mortality in critically ill patients with coronary heart disease accompanied by chronic kidney disease: a retrospective study using the MIMIC-IV database.Frontiers in cardiovascular medicine · 2024Article
- Phosphate and Coronary Artery Disease in Patients with Chronic Kidney Disease.Journal of atherosclerosis and thrombosis · 2024Review
- Serum Fibroblast Growth Factor 23 Levels are Associated with Vascular Smooth Muscle Dysfunction in Type 2 Diabetes.Journal of atherosclerosis and thrombosis · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the evolution of skeletons, terrestrial vertebrates acquired strong bones made of calcium-phosphate. By keeping the extracellular fluid in a supersaturated condition regarding calcium and phosphate ions, they created the bone when and where they wanted simply by providing a cue for precipitation. To secure this strategy, they acquired a novel endocrine system to strictly control the extracellular phosphate concentration. In response to phosphate intake, fibroblast growth factor-23 (FGF23) is secreted from the bone and acts on the kidney through binding to its receptor Klotho to increase urinary phosphate excretion, thereby maintaining phosphate homeostasis. The FGF23-Klotho endocrine system, when disrupted in mice, results in hyperphosphatemia and vascular calcification. Besides, mice lacking Klotho or FGF23 suffer from complex aging-like phenotypes, which are alleviated by placing them on a low- phosphate diet, indicating that phosphate is primarily responsible for the accelerated aging. Phosphate acquires the ability to induce cell damage and inflammation when precipitated with calcium. In the blood, calcium-phosphate crystals are adsorbed by serum protein fetuin-A and prevented from growing into large precipitates. Consequently, nanoparticles that comprised calcium-phosphate crystals and fetuin-A, termed calciprotein particles (CPPs), are generated and dispersed as colloids. CPPs increase in the blood with an increase in serum phosphate and age. Circulating CPP levels correlate positively with vascular stiffness and chronic non-infectious inflammation, raising the possibility that CPPs may be an endogenous pro-aging factor. Terrestrial vertebrates with the bone made of calcium- phosphate may be destined to age due to calcium-phosphate in the blood.
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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.