Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia
Autor: | Kerstin Amann, Kai-Uwe Eckardt, Jakob Voelkl, Florian Lang, Ioana Alesutan, Makoto Kuro-o, Andreas Pasch, Burkert Pieske |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Calcium Phosphates
Vascular smooth muscle Myocytes Smooth Muscle chemistry.chemical_element Phosphate Review Calcium Muscle Smooth Vascular 03 medical and health sciences Cellular and Molecular Neuroscience Hyperphosphatemia Chondrocytes medicine Extracellular Vascular smooth muscle cells CKD Animals Humans Renal Insufficiency Chronic Vascular Calcification Molecular Biology Vascular calcification Pharmacology 0303 health sciences Osteoblasts Receptor Activator of Nuclear Factor-kappa B business.industry RANK Ligand 030302 biochemistry & molecular biology Transdifferentiation NF-kappa B Cell Biology medicine.disease Gene Expression Regulation chemistry Osteogenic signaling Cell Transdifferentiation Cancer research Molecular Medicine Signal transduction business Intracellular Signal Transduction Calcification |
Zdroj: | Cellular and Molecular Life Sciences |
Popis: | 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. |
Databáze: | OpenAIRE |
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