The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Ferroptosis occurs through an osmotic mechanism and propagates independently of cell rupture
Open accessAbstract
Ferroptosis is a regulated form of necrotic cell death that is caused by the accumulation of oxidized phospholipids, leading to membrane damage and cell lysis1,2. Although other types of necrotic death such as pyroptosis and necroptosis are mediated by active mechanisms of execution3–6, ferroptosis is thought to result from the accumulation of unrepaired cell damage1. Previous studies have suggested that ferroptosis has the ability to spread through cell populations in a wave-like manner, resulting in a distinct spatiotemporal pattern of cell death7,8. Here we investigate the mechanism of ferroptosis execution and discover that ferroptotic cell rupture is mediated by plasma membrane pores, similarly to cell lysis in pyroptosis and necroptosis3,4. We further find that intercellular propagation of death occurs following treatment with some ferroptosis-inducing agents, including erastin2,9 and C′ dot nanoparticles8, but not upon direct inhibition of the ferroptosis-inhibiting enzyme glutathione peroxidase 4 (GPX4)10. Propagation of a ferroptosis-inducing signal occurs upstream of cell rupture and involves the spreading of a cell swelling effect through cell populations in a lipid peroxide- and iron-dependent manner. Two complementary studies from the laboratories of Riegman et al. and Katikaneni et al., respectively, identify a key role for controlled wave-like propagation of lipid peroxide signalling during wound detection in vivo and in ferroptotic cell death.
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Citations
Cites
Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
Dixon, S. J., Lemberg, K. M., Lamprecht, M. R., Skouta, R., Zaitsev, E. M., Gleason, C. E., Patel, D. N., Bauer, A. J., Cantley, A. M., Yang, W. S., et al. (2012) · Cell · doi:10.1016/j.cell.2012.03.042 · Cited by 18,691
Self-citationRegulation of Ferroptotic Cancer Cell Death by GPX4
Yang, W. S., SriRamaratnam, R., Welsch, M. E., Shimada, K., Skouta, R., Viswanathan, V. S., Cheah, J. H., Clemons, P. A., Shamji, A. F., Clish, C. B., et al. (2014) · Cell · doi:10.1016/j.cell.2013.12.010 · Cited by 7,713
Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
Stockwell, B. R., Friedmann Angeli, J. P., Bayir, H., Bush, A. I., Conrad, M., Dixon, S. J., Fulda, S., Gascón, S., Hatzios, S. K., Kagan, V. E., et al. (2017) · Cell · doi:10.1016/j.cell.2017.09.021 · Cited by 7,695
Self-citationGalluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
Self-citationThe CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis
Bersuker, K., Hendricks, J. M., Li, Z., Magtanong, L., Ford, B., Tang, P. H., Roberts, M. A., Tong, B., Maimone, T. J., Zoncu, R., et al. (2019) · Nature · doi:10.1038/s41586-019-1705-2 · Cited by 3,703
Self-citationFSP1 is a glutathione-independent ferroptosis suppressor
Doll, S., Freitas, F. P., Shah, R., Aldrovandi, M., da Silva, M. C., Ingold, I., Goya Grocin, A., Xavier da Silva, T. N., Panzilius, E., Scheel, C. H., et al. (2019) · Nature · doi:10.1038/s41586-019-1707-0 · Cited by 3,341
Ferroptosis: Death by Lipid Peroxidation
Yang, W. S., & Stockwell, B. R. (2016) · Trends in Cell Biology · doi:10.1016/j.tcb.2015.10.014 · Cited by 3,088
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
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Role of GPX4 in ferroptosis and its pharmacological implication
Seibt, T. M., Proneth, B., & Conrad, M. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.09.014 · Cited by 1,520
Cited by
The Cell Biology of Ferroptosis
Dixon, S. J., & Olzmann, J. A. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00703-5 · Cited by 1,596
Self-citationTargeting ferroptosis protects against experimental (multi)organ dysfunction and death
Van Coillie, S., Van San, E., Goetschalckx, I., Wiernicki, B., Mukhopadhyay, B., Tonnus, W., Choi, S. M., Roelandt, R., Dumitrascu, C., Lamberts, L., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-28718-6 · Cited by 186
Zhang, W., Dai, J., Hou, G., Liu, H., Zheng, S., Wang, X., Lin, Q., Zhang, Y., Lu, M., Gong, Y., et al. (2023) · Molecular Cell · doi:10.1016/j.molcel.2023.10.042 · Cited by 125
Van San, E., Debruyne, A. C., Veeckmans, G., Tyurina, Y. Y., Tyurin, V. A., Zheng, H., Choi, S. M., Augustyns, K., van Loo, G., Michalke, B., et al. (2023) · Cell Death & Differentiation · doi:10.1038/s41418-023-01195-0 · Cited by 103
“Phospholipids containing polyunsaturated fatty acids (PUFAs) are very susceptible to peroxidation, contributing to membrane permeabilization and cell lysis [13, 14].”
BackgroundSelective ferroptosis vulnerability due to familial Alzheimer’s disease presenilin mutations
Greenough, M. A., Lane, D. J. R., Balez, R., Anastacio, H. T. D., Zeng, Z., Ganio, K., McDevitt, C. A., Acevedo, K., Belaidi, A. A., Koistinaho, J., et al. (2022) · Cell Death & Differentiation · doi:10.1038/s41418-022-01003-1 · Cited by 102
Metadata
- Authors
- Riegman, M., Sagie, L., Galed, C., Levin, T., Steinberg, N., Dixon, S. J., Wiesner, U., Bradbury, M. S., Niethammer, P., Zaritsky, A., & Overholtzer, M.
- Venue
- Nature Cell Biology
- Published
- 2020-08-31
- Volume
- 22
- Issue
- 9
- Pages
- 1042-1048
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W3082740036
- Cited by
- 474
- References
- 31
- FWCI
- 24.63
- Type
- journal article
- Language
- en
- Open access
- green
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- Riegman, M., Sagie, L., Galed, C., Levin, T., Steinberg, N., Dixon, S. J., Wiesner, U., Bradbury, M. S., Niethammer, P., Zaritsky, A., & Overholtzer, M. (2020). Ferroptosis occurs through an osmotic mechanism and propagates independently of cell rupture. Nature Cell Biology. https://doi.org/10.1038/s41556-020-0565-1
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