Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-03-18

AUTHORS

Jakob Voelkl, Florian Lang, Kai-Uwe Eckardt, Kerstin Amann, Makoto Kuro-o, Andreas Pasch, Burkert Pieske, Ioana Alesutan

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. More... »

PAGES

2077-2091

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00018-019-03054-z

    DOI

    http://dx.doi.org/10.1007/s00018-019-03054-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112858468

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30887097


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