1. ‘Shedding’ light on mechanisms of hyperphosphatemic vascular dysfunction 
Dylan Burger, Adeera Levin 
Kidney International 
Volume 83, Issue 2, Pages (February 2013)
DOI: /ki
Copyright © 2013 International Society of Nephrology Terms and Conditions

2. Figure 1
Putative mechanisms by which phosphate influences vascular health and function. Phosphate (PO4–) promotes osteoblastic differentiation of vascular smooth muscle cells (VSMCs). In endothelial cells (ECs), PO4- induces the formation of microparticles, reduces angiogenesis and nitric oxide (NO) release, and increases the production of reactive oxygen species (ROS), inflammation, cell detachment, and apoptosis. The deleterious effects on ECs may be mediated through loss of annexin II during microparticle shedding. Processes in which the loss of annexin II signaling has been implicated are indicated in pink.
Kidney International  , DOI: ( /ki )
Copyright © 2013 International Society of Nephrology Terms and Conditions

3. Figure 2
Integrated flow of basic and clinical observations toward improved patient care. Relevant clinical and experimental milestones are identified in blue. Light gray blocks indicate observations relevant to hyperphosphatemia and endothelial health. Clinical and experimental observations have led to the hypothesis that elevated phosphate damages the endothelium via impaired annexin II–mediated signaling. Whether these mechanisms represent viable targets for improving patient health remains unclear.
Kidney International  , DOI: ( /ki )
Copyright © 2013 International Society of Nephrology Terms and Conditions