@article{ref1,
title="Heavy metal suicide",
journal="American journal of physiology. Renal physiology",
year="2017",
author="Linkermann, Andreas and Stockwell, Brent R. and Vanden Berghe, Tom",
volume="313",
number="4",
pages="F959-F960",
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).<br><br>Copyright © 2017, American Journal of Physiology-Renal Physiology.<p /> <p>Language: en</p>",
language="en",
issn="1931-857X",
doi="10.1152/ajprenal.00273.2017",
url="http://dx.doi.org/10.1152/ajprenal.00273.2017"
}