期刊
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
卷 474, 期 8, 页码 949-962出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00424-022-02688-6
关键词
Fetuin-A; Mineral chaperone; Biomineralization; Inflammation; Kidney injury
类别
资金
- University of Bern
- NCCR (National Center of Competence in Research) Kidney.CH grant of the Swiss National Science Foundation
- EU grant FP7 International Cooperation (People Cofund) [IKPP246539]
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [TRR 219, 322900939, 403041552]
Traditionally, fetuin-A is known as an anti-calcification protein that prevents cardiovascular calcification. Recent evidence suggests that it also plays a crucial role in moderating tissue inflammation and fibrosis, as well as serving as a systemic indicator of acute inflammatory disease. In this context, unbalanced depletion of fetuin-A may trigger a vicious cycle of progressive calcification, inflammation, and tissue injury.
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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