Citation

Linkermann A, Stockwell BR, Vanden Berghe T. Am. J. Physiol. Renal Physiol. 2017; 313(4): F959-F960.

Affiliation

Ghent University.

Copyright

(Copyright © 2017, American Physiological Society)

DOI

10.1152/ajprenal.00273.2017

PMID

28566503

Abstract

In acute kidney injury (AKI), the majority of dying tubular cells succumbs to an iron-dependent form of regulated necrosis, referred to as ferroptosis. Ferroptosis is essentially mediated by iron-catalyzed lipid peroxidation upon GPX4 dysfunction. Heme oxygenase 1 (HO-1) is a master regulator of intracellular free iron due to the conversion of heme to iron, carbon monoxide, and biliverdin(12), and therefore represents a potential regulator of ferroptotic cell death. In this issue of AJP - Renal Physiology, Adedoyin et al. demonstrate that the lack of HO-1 sensitizes renal tubular cells to ferroptosis(1).

Copyright © 2017, American Journal of Physiology-Renal Physiology.

Language: en

Keywords

Ferritin; Ferroptosis; Heme; Heme Oxygenase; Regulated Necrosis