A publisher's correction has been issued for an article in Nature regarding the role of oestradiol in inhibiting ferroptosis and acute kidney injury, initially published online August 13, 2025. The correction addresses errors introduced during the typesetting process that were not present in the peer-reviewed version of the manuscript or the original data.
The errors included incorrect chemical structures in Figure 2e and 2f, where the structure for 4OH-E2 was mistakenly shown instead of 17β-estradiol in Figure 2e, and in Figure 2f, the 2OH-E2 structure contained "H" instead of "HO" in the upper left corner. Discrepancies were also found in the sample sizes reported in Figure 2o, 2p, and 2q for Sham and IRI OVX mice, and incorrect references to Extended Data figures on pages 1011 and 1012.
According to the publisher's note, the errors do not affect the scientific conclusions of the study. The research explores the multiple functions of oestradiol, a primary female sex hormone, in mitigating ferroptosis, a form of cell death driven by iron and lipid peroxidation, and its subsequent impact on acute kidney injury. The study investigated the mechanisms by which oestradiol and its metabolites influence these processes, potentially opening new avenues for therapeutic interventions.
Ferroptosis has gained increasing attention in recent years as a key player in various diseases, including kidney disease, neurodegenerative disorders, and cancer. Understanding the factors that regulate ferroptosis could lead to the development of novel treatments targeting these conditions. The original article in Nature presented evidence of oestradiol's protective effects against ferroptosis-induced kidney damage in preclinical models.
The corrected article is now available on the Nature website. Researchers and clinicians in the fields of nephrology, endocrinology, and cell biology are advised to refer to the corrected version for accurate information. The publisher regrets the errors and any inconvenience they may have caused.
Discussion
Join the conversation
Be the first to comment