Department of Nephrology and Hypertension, Bern University Hospital, Freiburgstrasse 15, 3010, Bern, Switzerland.
Department of Biomedical Research, University of Bern, Freiburgstrasse 15, 3010, Bern, Switzerland.
Pflugers Arch. 2022 Aug;474(8):949-962. doi: 10.1007/s00424-022-02688-6. Epub 2022 Apr 11.
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.
传统上，胎球蛋白-A 是血液中典型的抗钙化蛋白，可防止心血管钙化。血清胎球蛋白-A 水平低通常与矿物质代谢失衡和终末期肾病患者死亡率升高有关。最近的证据表明，胎球蛋白-A 是调节组织炎症和纤维化的关键因素，也是全身性急性炎症疾病的指标。在此，我们将讨论胎球蛋白-A 在矿物质代谢和炎症生物学方面的扩展功能。在这种情况下，胎球蛋白-A 的不平衡耗竭可能是触发进行性钙化、炎症和组织损伤的恶性循环的关键事件。因此，我们将胎球蛋白-A 命名为组织伴侣，并提出了在外源性胎球蛋白-A 作为与内源性蛋白急性耗竭相关疾病的预防剂或紧急治疗的潜在用途。
