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Phosphate: an old bone molecule but new cardiovascular risk factor
Navid Shobeiri1, Michael A Adams, Rachel M Holden
1Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
British Journal of Clinical Pharmacology
|March 20, 2013
Summary
Phosphate balance is crucial for health, involving hormones and transporters. Imbalances can lead to disorders and vascular calcification, necessitating new therapeutic strategies.
Area of Science:
- Physiology
- Biochemistry
- Endocrinology
Background:
- Phosphate homeostasis is regulated by bone, parathyroid gland, and kidney hormones.
- Phosphate acts as a signaling molecule in bone formation, involving SLC34 and SLC20 transporter families.
- Phosphate imbalance can cause mineral disorders and vascular calcification.
Purpose of the Study:
- To review the physiological mechanisms of phosphate balance and cell signaling.
- To explore the pathological consequences of hyperphosphatemia.
- To discuss current and emerging therapeutics for hyperphosphatemia.
Main Methods:
- Literature review of physiological and pathological mechanisms.
- Analysis of phosphate transporter families (SLC34 and SLC20).
- Examination of hyperphosphatemia's role in mineral disorders and cardiovascular disease.
Main Results:
- Phosphate balance relies on precise regulation of gut and kidney phosphate transporters.
- Phosphate signaling in osteoblasts and vascular smooth muscle cells involves PiT1 and PiT2 (SLC20 family).
- Hyperphosphatemia is linked to extra-osseous calcification and cardiovascular disease in CKD-MBD.
Conclusions:
- Understanding phosphate transport and signaling is key to preventing mineral disorders.
- Effective management of hyperphosphatemia is essential for reducing cardiovascular risk.
- New therapeutic approaches are needed to address complex phosphate dysregulation.
Keywords:
SLC20 (PiT1 and 2)cardiovascular diseasechronic kidney diseasehyperphosphataemiaphosphatevascular calcificationMore Related Videos
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