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Comment
. 2019 Apr;29(4):263-264.
doi: 10.1038/s41422-019-0150-y.

Broken hearts: Iron overload, ferroptosis and cardiomyopathy

Marcus Conrad  1 , Bettina Proneth  2
Affiliations
Comment

Broken hearts: Iron overload, ferroptosis and cardiomyopathy

Marcus Conrad et al. Cell Res. 2019 Apr.
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Doxorubicin and ischemia/reperfusion injury (IRI) cause ferroptosis in cardiomyocytes and cardiomyopathy. Exposure of cardiac tissue to doxorubicin (or transient IRI) causes an NRF2-dependent upregulation of HMOX1, heme degradation, iron overload and associated lipid peroxidation, the latter two are hallmarks of ferroptosis. The iron-chelating agent dexrazoxane, the lipid peroxidation inhibiting compounds mitoTEMPO and Fer-1 robustly improve tissue damage inflicted by doxorubicin and IRI, thus warranting the development of ferroptosis inhibitors for the effective treatement of heart disease. ARE antioxidant response element, Fer-1 ferrostatin-1, HMOX1 heme oxygenase-1, mitoTEMPO 2-(2,2,6,6-Tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride, NRF2 Nuclear factor (erythroid-derived 2)-like 2
See this image and copyright information in PMC

Comment on

  • Ferroptosis as a target for protection against cardiomyopathy.
    Fang X, Wang H, Han D, Xie E, Yang X, Wei J, Gu S, Gao F, Zhu N, Yin X, Cheng Q, Zhang P, Dai W, Chen J, Yang F, Yang HT, Linkermann A, Gu W, Min J, Wang F. Fang X, et al. Proc Natl Acad Sci U S A. 2019 Feb 12;116(7):2672-2680. doi: 10.1073/pnas.1821022116. Epub 2019 Jan 28. Proc Natl Acad Sci U S A. 2019. PMID: 30692261 Free PMC article.

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