Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 76, Issue 11, Pages 2077-2091Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-019-03054-z
Keywords
Osteogenic signaling; Vascular smooth muscle cells; Vascular calcification; Phosphate; CKD
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Funding
- Johannes Kepler University Linz
- Berlin Institute of Health (BIH)
- Else Kroner-Fresenius-Stiftung
- Deutsche Forschungsgemeinschaft [AL2054/1-1, VO2259/2-1]
- DZHK (German Centre for Cardiovascular Research)
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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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