Rudloff, StefanStefanRudloffJahnen-Dechent, WilliWilliJahnen-DechentHuynh-Do, UyenUyenHuynh-Do0000-0002-7276-032X2024-10-092024-10-092022-08https://boris-portal.unibe.ch/handle/20.500.12422/70121Traditionally, 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.enBiomineralization Fetuin-A Inflammation Kidney injury Mineral chaperone600 - Technology::610 - Medicine & healtharticle10.48350/1692213540390610.1007/s00424-022-02688-6