ArticlePflugers Archiv : European journal of physiology2021
Increased β-adrenergic stimulation augments vascular smooth muscle cell calcification via PKA/CREB signalling.
Article in Pflugers Archiv : European journal of physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Role of Inositol Hexakisphosphate Kinases in Vascular Smooth Muscle Cell Calcification.International journal of molecular sciences · 2026Article
- Article
- Vasorelaxant effects of the edible flowersPharmaceutical biology · 2025Article
- Sphingosine kinase 1 inhibition aggravates vascular smooth muscle cell calcification.Pflugers Archiv : European journal of physiology · 2025Article
- Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.Aging · 2025Article
- Characterization of Circulating Vesicles of Complicated and Uncomplicated Systemic Sclerosis Patients and Their Role in Vascular Dysfunction.International journal of molecular sciences · 2025Article
- Phenotypic switch of vascular smooth muscle cells in COVID-19: Role of cholesterol, calcium, and phosphate.Journal of cellular physiology · 2024Review
- The Associations Between Abdominal Obesity and Coronary Artery Calcification in Chronic Kidney Disease Population.International journal of nephrology and renovascular disease · 2024Article
- Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling.Biomolecules · 2022Article
- Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells.Cells · 2021Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic kidney disease (CKD), hyperphosphatemia promotes medial vascular calcification, a process augmented by osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). VSMC function is regulated by sympathetic innervation, and these cells express α- and β-adrenergic receptors. The present study explored the effects of β2-adrenergic stimulation by isoproterenol on VSMC calcification. Experiments were performed in primary human aortic VSMCs treated with isoproterenol during control or high phosphate conditions. As a result, isoproterenol dose dependently up-regulated the expression of osteogenic markers core-binding factor α-1 (CBFA1) and tissue-nonspecific alkaline phosphatase (ALPL) in VSMCs. Furthermore, prolonged isoproterenol exposure augmented phosphate-induced calcification of VSMCs. Isoproterenol increased the activation of PKA and CREB, while knockdown of the PKA catalytic subunit α (PRKACA) or of CREB1 genes was able to suppress the pro-calcific effects of isoproterenol in VSMCs. β2-adrenergic receptor silencing or inhibition with the selective antagonist ICI 118,551 blocked isoproterenol-induced osteogenic signalling in VSMCs. The present observations imply a pro-calcific effect of β2-adrenergic overstimulation in VSMCs, which is mediated, at least partly, by PKA/CREB signalling. These observations may support a link between sympathetic overactivity in CKD and vascular calcification.
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