Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Voelkl J, Lang F, Eckardt KU, Amann KU, Kuro-o M, Pasch A, Pieske B, Alesutan I (2019)


Publication Type: Journal article, Review article

Publication year: 2019

Journal

DOI: 10.1007/s00018-019-03054-z

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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APA:

Voelkl, J., Lang, F., Eckardt, K.U., Amann, K.U., Kuro-o, M., Pasch, A.,... Alesutan, I. (2019). Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia. Cellular and Molecular Life Sciences. https://doi.org/10.1007/s00018-019-03054-z

MLA:

Voelkl, Jakob, et al. "Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia." Cellular and Molecular Life Sciences (2019).

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