ER Stress Controls Iron Metabolism Through Induction of Hepcidin

Author:

Vecchi Chiara1,Montosi Giuliana1,Zhang Kezhong2,Lamberti Igor1,Duncan Stephen A.3,Kaufman Randal J.4,Pietrangelo Antonello1

Affiliation:

1. Center for Hemochromatosis, Department of Internal Medicine, University Hospital Policlinico di Modena, Modena, Italy.

2. Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA.

3. Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

4. Howard Hughes Medical Institute, Departments of Biological Chemistry and Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109–0650, USA.

Abstract

Ironing Out Stress The peptide hormone, hepcidin, is secreted from the liver in response to extracellular factors, including inflammation, and regulates iron homeostasis by controlling transmembrane iron transport. Vecchi et al. (p. 877 ) showed that intracellular stress signals in the endoplasmic reticulum also control hepcidin expression and can thus modulate local or systemic iron traffic. This mechanism occurs through the transcription factor CREBH, which is a known mediator of the inflammatory response. Collectively, the results suggest a direct link between the intracellular stress response, innate immunity, and iron metabolism.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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