Abstract
Matrix vesicle (MV)-mediated mineralization is important for bone ossification. However, under certain circumstances such as atherosclerosis, mineralization may occur in the arterial wall. Bone-type tissue-nonspecific alkaline phosphatase (TNAP) hydrolyzes inorganic pyrophosphate (PPi) and generates inorganic phosphate (Pi), which is essential for MV-mediated hydroxyapatite formation. MVs contain another phosphatase, PHOSPHO1, that serves as an additional supplier of Pi. Activation of bone-type tissue-nonspecific alkaline phosphatase (TNAP) in vascular smooth muscle cells precedes vascular calcification. By degrading PPi, TNAP plays a procalcific role changing the Pi/PPi ratio toward mineralization. A pathologic role of bone-type TNAP and PHOSPHO1 make them to be attractive targets for cardiovascular therapy.
| Original language | English |
|---|---|
| Pages (from-to) | 5821-5828 |
| Number of pages | 8 |
| Journal | Current Pharmaceutical Design |
| Volume | 20 |
| Issue number | 37 |
| Publication status | Published - 2014 |
Keywords
- alkaline phosphatase
- atherosclerosis
- biomineralization
- vascular smooth muscle
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