Format

Send to

Choose Destination
Semin Nephrol. 2019 Jan;39(1):76-84. doi: 10.1016/j.semnephrol.2018.10.006.

Iron Homeostasis in Healthy Kidney and its Role in Acute Kidney Injury.

Author information

1
Center for Immunity, Inflammation and Regeneration Medicine, Division of Nephrology, University of Virginia, Charlottesville, VA.
2
Center for Immunity, Inflammation and Regeneration Medicine, Division of Nephrology, University of Virginia, Charlottesville, VA. Electronic address: swami@virginia.edu.

Abstract

Iron is required for key aspects of cellular physiology including mitochondrial function and DNA synthesis and repair. However, free iron is an aberration because of its ability to donate electrons, reduce oxygen, and generate reactive oxygen species. Iron-mediated cell injury or ferroptosis is a central player in the pathogenesis of acute kidney injury. There are several homeostatic proteins and pathways that maintain critical balance in iron homeostasis to allow iron's biologic functions yet avoid ferroptosis. Hepcidin serves as the master regulator of iron homeostasis through its ability to regulate ferroportin-mediated iron export and intracellular H-ferritin levels. Hepcidin is a protective molecule in acute kidney injury. Drugs targeting hepcidin, H-ferritin, and ferroptosis pathways hold great promise to prevent or treat kidney injury. In this review we discuss iron homeostasis under physiological and pathologic conditions and highlight its importance in acute kidney injury.

KEYWORDS:

Hepcidin; iron; ischemia-reperfusion; kidney; sepsis

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center