Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification.

Rudloff, Stefan; Jahnen-Dechent, Willi; Huynh-Do, Uyen (2022). Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification. Pflügers Archiv : European journal of physiology, 474(8), pp. 949-962. Springer 10.1007/s00424-022-02688-6

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Traditionally, fetuin-A embodies the prototype anti-calcification protein in the blood, preventing cardiovascular calcification. Low serum fetuin-A is generally associated with mineralization dysbalance and enhanced mortality in end stage renal disease. Recent evidence indicates that fetuin-A is a crucial factor moderating tissue inflammation and fibrosis, as well as a systemic indicator of acute inflammatory disease. Here, the expanded function of fetuin-A is discussed in the context of mineralization and inflammation biology. Unbalanced depletion of fetuin-A in this context may be the critical event, triggering a vicious cycle of progressive calcification, inflammation, and tissue injury. Hence, we designate fetuin-A as tissue chaperone and propose the potential use of exogenous fetuin-A as prophylactic agent or emergency treatment in conditions that are associated with acute depletion of endogenous protein.

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