Joanne L. Reynolds

TL;DR: In the context of raised Ca and P, vascular calcification is a modifiable, cell-mediated process regulated by vesicle release, and perturbation of the production or function of these inhibitors would lead to accelerated vascular calcifying.

TL;DR: A sequence of molecular events in vascular calcification is suggested beginning with the loss of expression by vascular smooth muscle cells, of constitutive inhibitory proteins, and ending with expression by VSMCs and macrophages of chondrocytic, osteoblastic, and osteoclastic-associated proteins that orchestrate the calcification process.

TL;DR: Evidence is provided that the uptake of the serum protein fetuin-A by VSMC is a key event in the inhibition of vesicle-mediated VSMC calcification, a condition associated with an elevated circulating calcium x phosphate product in patients with ESRD.

TL;DR: In contrast to the coordinated signaling response observed in chondrocyte MVs, mineralization of VSMC-MVs is a pathological response to disturbed intracellular calcium homeostasis that leads to inhibitor depletion and the formation of AnxA6/phosphatidylserine nucleation complexes.

TL;DR: In this article, the authors found that Gamma-carboxlyated coagulation proteins are potent inhibitors of vascular calcification suggesting warfarin action on these factors also contributes to accelerated calcification in patients receiving this drug.