The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Necrostatin-1 Reduces Histopathology and Improves Functional Outcome after Controlled Cortical Impact in Mice
Open accessAbstract
Necroptosis is a newly identified type of programmed necrosis initiated by the activation of tumor necrosis factor alpha (TNFα)/Fas. Necrostatin-1 is a specific inhibitor of necroptosis that reduces ischemic tissue damage in experimental stroke models. We previously reported decreased tissue damage and improved functional outcome after controlled cortical impact (CCI) in mice deficient in TNFα and Fas. Hence, we hypothesized that necrostatin-1 would reduce histopathology and improve functional outcome after CCI in mice. Compared with vehicle-/inactive analog-treated controls, mice administered necrostatin-1 before CCI had decreased propidium iodide-positive cells in the injured cortex and dentate gyrus (6 h), decreased brain tissue damage (days 14, 35), improved motor (days 1 to 7), and Morris water maze performance (days 8 to 14) after CCI. Improved spatial memory was observed even when drug was administered 15 mins after CCI. Necrostatin-1 treatment did not reduce caspase-3-positive cells in the dentate gyrus or cortex, consistent with a known caspase-independent mechanism of necrostatin-1. However, necrostatin-1 reduced brain neutrophil influx and microglial activation at 48 h, suggesting a novel anti-inflammatory effect in traumatic brain injury (TBI). The data suggest that necroptosis plays a significant role in the pathogenesis of cell death and functional outcome after TBI and that necrostatin-1 may have therapeutic potential for patients with TBI.
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Cites
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
Degterev, A., Huang, Z., Boyce, M., Li, Y., Jagtap, P., Mizushima, N., Cuny, G. D., Mitchison, T. J., Moskowitz, M. A., & Yuan, J. (2005) · Nature Chemical Biology · doi:10.1038/nchembio711 · Cited by 3,068
Self-citationHoller, N., Zaru, R., Micheau, O., Thome, M., Attinger, A., Valitutti, S., Bodmer, J.-L., Schneider, P., Seed, B., & Tschopp, J. (2000) · Nature Immunology · doi:10.1038/82732 · Cited by 1,938
Vercammen, D., Beyaert, R., Denecker, G., Goossens, V., Van Loo, G., Declercq, W., Grooten, J., Fiers, W., & Vandenabeele, P. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.187.9.1477 · Cited by 922
Dual Signaling of the Fas Receptor: Initiation of Both Apoptotic and Necrotic Cell Death Pathways
Vercammen, D., Brouckaert, G., Denecker, G., Van de Craen, M., Declercq, W., Fiers, W., & Vandenabeele, P. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.188.5.919 · Cited by 556
Caspase‐3 Mediated Neuronal Death After Traumatic Brain Injury in Rats
Clark, R. S. B., Kochanek, P. M., Watkins, S. C., Chen, M., Dixon, C. E., Seidberg, N. A., Melick, J., Loeffert, J. E., Nathaniel, P. D., Jin, K. L., et al. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.740740.x · Cited by 405
In situ immunodetection of activated caspase-3 in apoptotic neurons in the developing nervous system
Srinivasan, A., Roth, K. A., Sayers, R. O., Shindler, K. S., Wong, A. M., Fritz, L. C., & Tomaselli, K. J. (1998) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4400449 · Cited by 368
Apoptotic and necrotic cell death induced by death domain receptors
Denecker, G., Vercammen, D., Declercq, W., & Vandenabeele, P. (2001) · Cellular and Molecular Life Sciences · doi:10.1007/pl00000863 · Cited by 279
Zhang, X., Chen, J., Graham, S. H., Du, L., Kochanek, P. M., Draviam, R., Guo, F., Nathaniel, P. D., Szabó, C., Watkins, S. C., et al. (2002) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2002.00975.x · Cited by 254
Necrotic Death Pathway in FAS Receptor Signaling
Matsumura, H., Shimizu, Y., Ohsawa, Y., Kawahara, A., Uchiyama, Y., & Nagata, S. (2000) · The Journal of Cell Biology · doi:10.1083/jcb.151.6.1247 · Cited by 240
Structure–activity relationship study of novel necroptosis inhibitors
Teng, X., Degterev, A., Jagtap, P., Xing, X., Choi, S., Denu, R., Yuan, J., & Cuny, G. D. (2005) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2005.07.077 · Cited by 237
Self-citation
Cited by
Molecular mechanisms of necroptosis: an ordered cellular explosion
Vandenabeele, P., Galluzzi, L., Vanden Berghe, T., & Kroemer, G. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2970 · Cited by 2,382
Regulated necrosis: the expanding network of non-apoptotic cell death pathways
Berghe, T. V., Linkermann, A., Jouan-Lanhouet, S., Walczak, H., & Vandenabeele, P. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3737 · Cited by 1,735
Cellular Stress Responses: Cell Survival and Cell Death
Fulda, S., Gorman, A. M., Hori, O., & Samali, A. (2010) · International Journal of Cell Biology · doi:10.1155/2010/214074 · Cited by 1,519
The far-reaching scope of neuroinflammation after traumatic brain injury
Simon, D. W., McGeachy, M. J., Bayır, H., Clark, R. S. B., Loane, D. J., & Kochanek, P. M. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2017.13 · Cited by 1,190
Fricker, M., Tolkovsky, A. M., Borutaite, V., Coleman, M., & Brown, G. C. (2018) · Physiological Reviews · doi:10.1152/physrev.00011.2017 · Cited by 1,108
Metadata
- Authors
- You, Z., Savitz, S. I., Yang, J., Degterev, A., Yuan, J., Cuny, G. D., Moskowitz, M. A., & Whalen, M. J.
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2008-05-21
- Volume
- 28
- Issue
- 9
- Pages
- 1564-1573
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W1983078635
- Cited by
- 269
- References
- 33
- FWCI
- 7.86
- Type
- journal article
- Language
- en
- Open access
- green
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- You, Z., Savitz, S. I., Yang, J., Degterev, A., Yuan, J., Cuny, G. D., Moskowitz, M. A., & Whalen, M. J. (2008). Necrostatin-1 Reduces Histopathology and Improves Functional Outcome after Controlled Cortical Impact in Mice. Journal of Cerebral Blood Flow & Metabolism. https://doi.org/10.1038/jcbfm.2008.44
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
