The DOI matches its Crossref record; 454 of the 454 references it cites were found in a registry or an index.
Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications
Abstract
Ischemic stroke caused by arterial occlusion is the most common type of stroke, which is among the most frequent causes of disability and death worldwide. Current treatment approaches involve achieving rapid reperfusion either pharmacologically or surgically, both of which are time‐sensitive; moreover, blood flow recanalization often causes ischemia/reperfusion injury. However, even though neuroprotective intervention is urgently needed in the event of stroke, the exact mechanisms of neuronal death during ischemic stroke are still unclear, and consequently, the capacity for drug development has remained limited. Multiple cell death pathways are implicated in the pathogenesis of ischemic stroke. Here, we have reviewed these potential neuronal death pathways, including intrinsic and extrinsic apoptosis, necroptosis, autophagy, ferroptosis, parthanatos, phagoptosis, and pyroptosis. We have also reviewed the latest results of pharmacological studies on ischemic stroke and summarized emerging drug targets with a focus on clinical trials. These observations may help to further understand the pathological events in ischemic stroke and bridge the gap between basic and translational research to reveal novel neuroprotective interventions.
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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
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
Vander Heiden, M. G., Cantley, L. C., & Thompson, C. B. (2009) · Science · doi:10.1126/science.1160809 · Cited by 16,197
Apoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics
Kerr, J. F. R., Wyllie, A. H., & Currie, A. R. (1972) · British Journal of Cancer · doi:10.1038/bjc.1972.33 · Cited by 15,725
Regulation 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
mTOR Signaling in Growth, Metabolism, and Disease
Saxton, R. A., & Sabatini, D. M. (2017) · Cell · doi:10.1016/j.cell.2017.02.004 · Cited by 7,555
Ferroptosis: mechanisms, biology and role in disease
Jiang, X., Stockwell, B. R., & Conrad, M. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00324-8 · Cited by 7,505
Targeting HIF-1 for cancer therapy
Semenza, G. L. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1187 · Cited by 6,717 · cited 1×
“endothelial growth factor and erythropoietin (EPO), function to promote and increase oxygen delivery to hypoxic regions.(146,147) HIF‐1 responds to systemic oxygen levels by undergoing conformational changes and induces transcription by associating with hypoxia response elements in the promoters of hypoxia response ge…”
BackgroundThrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke
Hacke, W., Kaste, M., Bluhmki, E., Brozman, M., Dávalos, A., Guidetti, D., Larrue, V., Lees, K. R., Medeghri, Z., Machnig, T., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0804656 · Cited by 6,684 · cited 1×
“However, the proteolytic activities of r‐tPA can induce side effects such as blood‐brain barrier breakdown and intracranial hemorrhage,(338) and reduce the therapeutic time window.(339) I/R injury is also a common occurrence after blood flow is restored,340‐342 which is why the identification of novel neuroprotectants…”
BackgroundResting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827
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Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion
Tuo, Q.-Z., Liu, Y., Xiang, Z., Yan, H.-F., Zou, T., Shu, Y., Ding, X.-L., Zou, J.-J., Xu, S., Tang, F., et al. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-00917-z · Cited by 330
Self-citationWu, C., Zhang, S., Sun, H., Li, A., Hou, F., Qi, L., & Liao, H. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03086-8 · Cited by 54
Self-citationZhang, Q., Yi, Y., Chen, T., Ai, Y., Chen, Z., Liu, G., Tang, Z., Chen, J., Xu, T., Chen, X., et al. (2025) · Journal of Nanobiotechnology · doi:10.1186/s12951-025-03390-2 · Cited by 27
The Role of the Complement System in Synaptic Pruning after Stroke
Liu, H., Jiang, M., Chen, Z., Li, C., Yin, X., Zhang, X., & Wu, M. (2024) · Aging and disease · doi:10.14336/ad.2024.0373 · Cited by 14
Metadata
- Authors
- Tuo, Q., Zhang, S., & Lei, P.
- Venue
- Medicinal Research Reviews
- Publisher
- Wiley
- Published
- 2021-05-06
- Volume
- 42
- Issue
- 1
- Pages
- 259-305
- ISSN
- 0198-6325 (ISSN-L)
- 1098-1128
- OpenAlex
- W3157643617
- Cited by
- 728
- References
- 454
- FWCI
- 27.10
- Type
- journal article
- Language
- en
- Open access
- closed
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