ReviewCellular and molecular life sciences : CMLS2019
Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia.
Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.
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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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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
156 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.
- Hydrogen Sulfide and Oxygen Homeostasis in Atherosclerosis: A Systematic Review from Molecular Biology to Therapeutic Perspectives.International journal of molecular sciences · 2023Pooled it
- Risk factors associated with treatment failure in peritoneal dialysis-associated peritonitis.Experimental and therapeutic medicine · 2026Article
- 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
- Phosphate: An Anion Controlling Metabolic Functions.Nutrients · 2026Review
- Corylin Confers Vasoprotection via JDP2-Nrf2 Antioxidant Axis against Chronic Kidney Disease-Induced Smooth Muscle Cell Remodelling.Journal of cellular and molecular medicine · 2026Article
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- Meta-analysis of the impact of serum phosphorus reduction on the prognosis of non-dialysis CKD patients: evidence based on clinical outcomes.International urology and nephrology · 2026Review
- Secreted frizzled-related protein 1 augments vascular smooth muscle cell calcification via activating the Wnt/β-catenin/Runx2 axis.International urology and nephrology · 2026Article
- FGF-23 and Long-term Outcome in Peripheral Artery Disease.Angiology · 2026Article
- Broken signals: when the mineralostat alters the cardiovascular system.Pediatric nephrology (Berlin, Germany) · 2026Review
- HSP90AA1 Facilitates Vascular Calcification in Chronic Kidney Disease Involving Chaperone-Mediated Autophagy.Biomedicines · 2026Article
- Role and mechanism of G9A-BMP2 in calcification-induced formation of unstable plaque.Atherosclerosis plus · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Bilayer vascular grafts separately loaded with sodium copper chlorophyllin and keratin-based hydrogen sulfide donor with pro-endothelialization, anti-thrombogenicity, anti-inflammation, and anti-calcification properties.Bioactive materials · 2026Article
- Decoding vascular calcification: mechanistic insights and translational strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Differential gene expression in peripheral vascular smooth muscle cells of patients with peripheral artery disease.Clinical and experimental nephrology · 2026Article
- Role of Inositol Hexakisphosphate Kinases in Vascular Smooth Muscle Cell Calcification.International journal of molecular sciences · 2026Article
- Underlying Mechanisms of Osteoporosis in the Context of Multimorbidity: Clinical Challenges and Management Strategies.Nutrients · 2026Review
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
96 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 7 institutions in 3 countries.
Funding
Abstract
Medial vascular calcification has emerged as a putative key factor contributing to the excessive cardiovascular mortality of patients with chronic kidney disease (CKD). Hyperphosphatemia is considered a decisive determinant of vascular calcification in CKD. A critical role in initiation and progression of vascular calcification during elevated phosphate conditions is attributed to vascular smooth muscle cells (VSMCs), which are able to change their phenotype into osteo-/chondroblasts-like cells. These transdifferentiated VSMCs actively promote calcification in the medial layer of the arteries by producing a local pro-calcifying environment as well as nidus sites for precipitation of calcium and phosphate and growth of calcium phosphate crystals. Elevated extracellular phosphate induces osteo-/chondrogenic transdifferentiation of VSMCs through complex intracellular signaling pathways, which are still incompletely understood. The present review addresses critical intracellular pathways controlling osteo-/chondrogenic transdifferentiation of VSMCs and, thus, vascular calcification during hyperphosphatemia. Elucidating these pathways holds a significant promise to open novel therapeutic opportunities counteracting the progression of vascular calcification in CKD.
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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.