Correction: Fisher-Bautista et al. Genetic Markers Associated with Ferroptosis in Cardiovascular Diseases. Future Pharmacol. 2025, 5, 37

Text Correction

There was an error in the original publication [1]. The original version cited a retracted paper listed as reference number 41 (Ma, S.; Sun, L.; Wu, W.; Wu, J.; Sun, Z.; Ren, J. USP22 Protects Against Myocardial Ischemia–Reperfusion Injury via the SIRT1-p53/SLC7A11–Dependent Inhibition of Ferroptosis–Induced Cardiomyocyte Death. Front. Physiol. 2020, 11, 551318. Available online: https://www.frontiersin.org/articles/10.3389/fphys.2020.551318/full (accessed on 12 November 2024)). This citation has now been removed.

A correction has been made to Section 3, Paragraph 3:

Interestingly, the latest evidence is supported by other research: for example, Gao et al. demonstrated that transferrin transport and glutaminolysis promote ferroptosis triggered by complete amino acid or cysteine deprivation. Due to this group’s identification of glutaminolysis as a ferroptosis inducer, they used compound 968, a glutaminolysis inhibitor, to reduce myocardial IRI in an ex vivo cardiac model [39]. Indeed, they found that at the end of reperfusion, hearts treated with compound 968 or deferoxamine (DFO, an iron chelator and ferroptosis inhibitor) improved cardiac function. Ferroptosis is significantly more present in myocardial reperfusion than in ischemia, where markers of ferroptosis in ischemic injury such as acyl-CoA synthase long chain family member 4 (ACSL4), GPX4, iron, and MDA were not significant, but not in myocardial reperfusion, which showed elevated levels of ACSL4, iron, and MDA associated with decreased GPX4 [39]. Interestingly, the reduction of ferroptosis with DFO was observed in rat hearts subjected to I/R compared to ischemia-treated rat hearts [40].

References

With this correction, the order of some references has been adjusted accordingly. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.