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The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification.

The Journal of clinical investigation

alpha-2-HS-Glycoprotein, administration & dosage, Vitamin D, Species Specificity, Minerals, Mice, Knockout, Mice, Inbred DBA, Mice, Inbred C57BL, Mice, Male, complications, Kidney Failure, Chronic, Humans, Female, adverse effects, Diet, prevention & control, etiology, blood, Calciphylaxis, pathology, Calcinosis, physiology, genetics, deficiency, Blood Proteins, Animals

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      Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-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.

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