The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Ferroptotic cell death and TLR4/Trif signaling initiate neutrophil recruitment after heart transplantation
Open accessAbstract
Non-apoptotic forms of cell death can trigger sterile inflammation through the release of danger-associated molecular patterns, which are recognized by innate immune receptors. However, despite years of investigation the mechanisms which initiate inflammatory responses after heart transplantation remain elusive. Here, we demonstrate that ferrostatin-1 (Fer-1), a specific inhibitor of ferroptosis, decreases the level of pro-ferroptotic hydroperoxy-arachidonoyl-phosphatidylethanolamine, reduces cardiomyocyte cell death and blocks neutrophil recruitment following heart transplantation. Inhibition of necroptosis had no effect on neutrophil trafficking in cardiac grafts. We extend these observations to a model of coronary artery ligation-induced myocardial ischemia reperfusion injury where inhibition of ferroptosis resulted in reduced infarct size, improved left ventricular systolic function, and reduced left ventricular remodeling. Using intravital imaging of cardiac transplants, we uncover that ferroptosis orchestrates neutrophil recruitment to injured myocardium by promoting adhesion of neutrophils to coronary vascular endothelial cells through a TLR4/TRIF/type I IFN signaling pathway. Thus, we have discovered that inflammatory responses after cardiac transplantation are initiated through ferroptotic cell death and TLR4/Trif-dependent signaling in graft endothelial cells. These findings provide a platform for the development of therapeutic strategies for heart transplant recipients and patients, who are vulnerable to ischemia reperfusion injury following restoration of coronary blood flow.
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Citations
Cites
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Neutrophil recruitment and function in health and inflammation
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Self-citationInactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice
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BackgroundSelf-citationFerroptosis, but Not Necroptosis, Is Important in Nephrotoxic Folic Acid–Induced AKI
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Cited by
Ferroptosis: past, present and future
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The molecular and metabolic landscape of iron and ferroptosis in cardiovascular disease
Fang, X., Ardehali, H., Min, J., & Wang, F. (2023) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00735-4 · Cited by 1,081
The emerging role of ferroptosis in inflammation
Sun, Y., Chen, P., Zhai, B., Zhang, M., Xiang, Y., Fang, J., Xu, S., Gao, Y., Chen, X., Sui, X., et al. (2020) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2020.110108 · Cited by 739
Iron Homeostasis and Ferroptosis in Human Diseases: Mechanisms and Therapeutic Prospects
Ru, Q., Li, Y., Chen, L., Wu, Y., Min, J., & Wang, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01969-z · Cited by 724
Metadata
- Authors
- Li, W., Feng, G., Gauthier, J. M., Lokshina, I., Higashikubo, R., Evans, S., Liu, X., Hassan, A., Tanaka, S., Cicka, M., Hsiao, H.-M., Ruiz-Perez, D., Bredemeyer, A., Gross, R. W., Mann, D. L., Tyurina, Y. Y., Gelman, A. E., Kagan, V. E., Linkermann, A., Lavine, K. J., & Kreisel, D.
- Venue
- Journal of Clinical Investigation
- Published
- 2019-04-29
- Volume
- 129
- Issue
- 6
- Pages
- 2293-2304
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W2916144846
- Cited by
- 492
- References
- 12
- FWCI
- 35.09
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Li, W., Feng, G., Gauthier, J. M., Lokshina, I., Higashikubo, R., Evans, S., Liu, X., Hassan, A., Tanaka, S., Cicka, M., Hsiao, H.-M., Ruiz-Perez, D., Bredemeyer, A., Gross, R. W., Mann, D. L., Tyurina, Y. Y., Gelman, A. E., Kagan, V. E., Linkermann, A., . . . Kreisel, D. (2019). Ferroptotic cell death and TLR4/Trif signaling initiate neutrophil recruitment after heart transplantation. Journal of Clinical Investigation. https://doi.org/10.1172/jci126428
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