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Correction: Oestradiol's Role in Kidney Injury Research Clarified

A publisher's correction has been issued for a research 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 that occurred during the typesetting process, according to the publisher, and clarifies that these errors do not affect the scientific conclusions of the study.

The errors primarily involved the incorrect representation of chemical structures in figures and discrepancies in sample sizes reported in figure legends. Specifically, in Figure 2e, the structure for 4OH-E2 was mistakenly displayed instead of 17β-estradiol. Figure 2f contained an error in the 2OH-E2 structure, where H appeared instead of HO in the upper left portion. In Figures 2o, 2p, and 2q, the sample sizes for Sham and IRI OVX mice were initially reported incorrectly. Furthermore, the correction notes that Extended Data Figures 2ac, 2d, and 2e were incorrectly referenced as Extended Data Figures 3ac, 3d, and 3e in the text.

Ferroptosis, a form of regulated cell death driven by iron and lipid peroxidation, is an area of increasing interest in biomedical research. The original article explored the potential of oestradiol, a primary female sex hormone, in mitigating ferroptosis and subsequent acute kidney injury. Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days. AKI causes a buildup of waste products in the blood and makes it hard for kidneys to keep the right balance of fluid in the body.

Researchers in the field suggest that understanding the mechanisms by which oestradiol influences ferroptosis could lead to the development of new therapeutic strategies for preventing or treating AKI and other related conditions. The publisher's note emphasizes that the corrected figures and references now accurately reflect the peer-reviewed version of the manuscript and the original data. The publisher has not commented beyond the published correction.

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