Renal-specific loss of ferroportin disrupts iron homeostasis and attenuates recovery from acute kidney injury

Author:

Soofi Abdul1,Li Vivie1,Beamish Jeffrey A.2ORCID,Abdrabh Sham3,Hamad Mawieh3ORCID,Das Nupur K.4ORCID,Shah Yatrik M.24ORCID,Dressler Gregory R.1ORCID

Affiliation:

1. Department of Pathology, University of Michigan, Ann Arbor, Michigan, United States

2. Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States

3. Department of Medical Laboratory Sciences, University of Sharjah, Sharjah, United Arab Emirates

4. Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, United States

Abstract

Physiological iron homeostasis depends in part on renal resorption and export into the plasma. We show that specific deletion of iron exporters in the proximal tubules sensitizes cells to injury and inhibits recovery. This can promote a chronic kidney disease phenotype. Our paper demonstrates the need for iron balance in the proximal tubules to maintain and promote healthy recovery after acute kidney injury.

Funder

HHS | NIH | National Cancer Institute

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Fulbright scholarship

Audrey and Josh Rumsey

Publisher

American Physiological Society

Subject

Physiology

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