The serum protein α2–Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification
By C. Schäfer, A. Heiss, A. Schwarz, R. Westenfeld, M. Ketteler, Jürgen Floege, Werner Müller-Esterl, T. Schinke, W. Jahnen-Dechent. 2003
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Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein α2–Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D–rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.
Subfields: Genetics, Nephrology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/82af2aa33bccca69d0bdf0645ce1c1331d5efc22
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Citations in the corpus
- Emerging biomarkers for evaluating cardiovascular risk in the chronic kidney disease patient: how do new pieces fit into the uremic puzzle? (2008, background): “of Ca and PO4 are surely not the only factors influencing ectopic ossification in CKD (154).”