1,2, 4-Trimethoxybenzene Selectively Inhibits NLRP3 Inflammasome Activation and Attenuates Experimental Autoimmune Encephalomyelitis

Researchers showed that 1,2,4-TTB (1 mM) markedly suppressed nigericin- or ATP-induced NLRP3 inflammasome activation, thus decreased caspase-1 activation and IL-1β secretion in immortalized murine bone marrow-derived macrophages (iBMDMs) and in primary mouse microglia.
[Acta Pharmacologica Sinica]
1,2,4-Trimethoxybenzene selectively inhibits NLRP3 inflammasome activation and attenuates experimental autoimmune encephalomyelitis | Acta Pharmacologica Sinica. (n.d.). Retrieved March 1, 2021, from https://www.nature.com/articles/s41401-021-00613-8 Cite
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The Key Regulator of Necroptosis, RIP1 Kinase, Contributes to the Formation of Astrogliosis and Glial Scar in Ischemic Stroke

In a transient middle cerebral artery occlusion rat model and an oxygen and glucose deprivation and reoxygenation induced astrocytic injury model, the authors showed that receptor-interacting protein 1 (RIP1) kinase was significantly elevated in the reactive astrocytes.
[Translational Stroke Research]
Zhu, Y.-M., Lin, L., Wei, C., Guo, Y., Qin, Y., Li, Z.-S., Kent, T. A., McCoy, C. E., Wang, Z.-X., Ni, Y., Zhou, X.-Y., & Zhang, H.-L. (2021). The Key Regulator of Necroptosis, RIP1 Kinase, Contributes to the Formation of Astrogliosis and Glial Scar in Ischemic Stroke. Translational Stroke Research. https://doi.org/10.1007/s12975-021-00888-3 Cite
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Mesenchymal Stromal Cells Attenuate Post-Stroke Infection by Preventing Caspase-1-Dependent Splenic Marginal Zone B Cell Death

Scientists showed that intravenously administered MSCs preferentially migrate to the marginal zone (MZ) of the spleen, preserving injured MZ B cells and ameliorating post-stroke infection and mortality in the mouse middle cerebral artery occlusion model of acute ischemic stroke.
[Signal Transduction and Targeted Therapy]
Huang, Y., Wang, J., Lai, X., Qiu, Y., Cai, J., Ma, Y., Liu, Y., Qiu, W., Lu, Z., & Xiang, A. P. (2021). Mesenchymal stromal cells attenuate post-stroke infection by preventing caspase-1-dependent splenic marginal zone B cell death. Signal Transduction and Targeted Therapy, 6(1), 1–3. https://doi.org/10.1038/s41392-020-00415-0 Cite
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Influence of Height on Endothelial Maintenance Activity: A Narrative Review

Scientists explain some of the reasons that implicate hypertension as a major risk factor for stroke among the Japanese population.
[Environmental Health and Preventive Medicine]
Shimizu, Y., & Maeda, T. (2021). Influence of height on endothelial maintenance activity: a narrative review. Environmental Health and Preventive Medicine, 26(1), 19. https://doi.org/10.1186/s12199-021-00941-5 Cite
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An Arylthiazyne Derivative Is a Potent Inhibitor of Lipid Peroxidation and Ferroptosis Providing Neuroprotection In Vitro and In Vivo

Researchers showed that a condensed benzo[b]thiazine derivative small molecule with an arylthiazine backbone inhibited tert-Butyl hydroperoxide-induced lipid peroxidation and protected against ferroptotic cell death triggered by glutathione depletion or glutathione peroxidase 4 inhibition in neuronal cell lines.
[Scientific Reports]
Keuters, M. H., Keksa-Goldsteine, V., Dhungana, H., Huuskonen, M. T., Pomeshchik, Y., Savchenko, E., Korhonen, P. K., Singh, Y., Wojciechowski, S., Lehtonen, Š., Kanninen, K. M., Malm, T., Sirviö, J., Muona, A., Koistinaho, M., Goldsteins, G., & Koistinaho, J. (2021). An arylthiazyne derivative is a potent inhibitor of lipid peroxidation and ferroptosis providing neuroprotection in vitro and in vivo. Scientific Reports, 11(1), 3518. https://doi.org/10.1038/s41598-021-81741-3 Cite
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Developmental Synaptic Regulator, TWEAK/Fn14 Signaling, Is a Determinant of Synaptic Function in Models of Stroke and Neurodegeneration

By combining electrophysiological and phosphoproteomic approaches, scientists showed that TWEAK acutely dampened basal synaptic transmission and plasticity through neuronal Fn14 and impacted the phosphorylation state of pre- and postsynaptic proteins in adult mouse hippocampal slices.
[Proceedings of the National Academy of Sciences of the United States of America]
Nagy, D., Ennis, K. A., Wei, R., Su, S. C., Hinckley, C. A., Gu, R.-F., Gao, B., Massol, R. H., Ehrenfels, C., Jandreski, L., Thomas, A. M., Nelson, A., Gyoneva, S., Hajós, M., & Burkly, L. C. (2021). Developmental synaptic regulator, TWEAK/Fn14 signaling, is a determinant of synaptic function in models of stroke and neurodegeneration. Proceedings of the National Academy of Sciences, 118(6). https://doi.org/10.1073/pnas.2001679118 Cite
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Notch Signaling-Modified Mesenchymal Stem Cells Improve Tissue Perfusion by Induction of Arteriogenesis in a Rat Hindlimb Ischemia Model

In Sprague–Dawley rats, hindlimb ischemia was generated by femoral artery removal, then seven days after ischemic induction 1 × 105 SB623 cells or PBS was injected into the ischemic adductor muscle.
[Scientific Reports]
Maeda, S., Miyagawa, S., Kawamura, T., Shibuya, T., Watanabe, K., Nakagawa, T., Harada, A., Chida, D., & Sawa, Y. (2021). Notch signaling-modified mesenchymal stem cells improve tissue perfusion by induction of arteriogenesis in a rat hindlimb ischemia model. Scientific Reports, 11(1), 2543. https://doi.org/10.1038/s41598-021-82284-3 Cite
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Human Umbilical Cord Mesenchymal Stem Cell-Derived Exosomal miR-146a-5p Reduces Microglial-Mediated Neuroinflammation via Suppression of the IRAK1/TRAF6 Signaling Pathway after Ischemic Stroke

The authors found that injected human umbilcal cord-derived exosomes were able to access the site of ischemic damage and could be internalized by cells both in vivo and in vitro.
[Aging-Us]
Aging | Human umbilical cord mesenchymal stem cell-derived exosomal miR-146a-5p reduces microglial-mediated neuroinflammation via suppression of the IRAK1/TRAF6 signaling pathway after ischemic stroke - Full Text. (n.d.). Retrieved January 27, 2021, from https://www.aging-us.com/article/202466/text Cite
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Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes

Mitochondria can be released by astrocytes as part of a help-me signaling process in stroke. Scientists investigated the molecular mechanisms that underlay mitochondria secretion, redox status, and functional regulation in the extracellular environment.
[Translational Stroke Research]
Park, J.-H., Lo, E. H., & Hayakawa, K. (2021). Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes. Translational Stroke Research. https://doi.org/10.1007/s12975-021-00892-7 Cite
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Treatment with Atorvastatin During Vascular Remodeling Promotes Pericyte-Mediated Blood-Brain Barrier Maturation Following Ischemic Stroke

Scientists examined the hypothesis that, during vascular remodeling after stroke, treatment with atorvastatin could facilitate blood-brain barrier maturation in remodeling vasculature in ischemic brain.
[Translational Stroke Research]
Yang, Y., Yang, L. Y., Salayandia, V. M., Thompson, J. F., Torbey, M., & Yang, Y. (2021). Treatment with Atorvastatin During Vascular Remodeling Promotes Pericyte-Mediated Blood-Brain Barrier Maturation Following Ischemic Stroke. Translational Stroke Research. https://doi.org/10.1007/s12975-020-00883-0 Cite
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Reparative System Arising from CCR2(+) Monocyte Conversion Attenuates Neuroinflammation following Ischemic Stroke

Scientists found that CCR2highCX3CR1low monocytes recruited to the injured brain were cytokine-dependently converted into CCR2lowCX3CR1high macrophages, especially under the influence of IL-4 and IL-13, thereby attenuating the neuroinflammation following sterile ischemic stroke.
[Translational Stroke Research]
Park, J., Kim, J. Y., Kim, Y. R., Huang, M., Chang, J. Y., Sim, A. Y., Jung, H., Lee, W. T., Hyun, Y.-M., & Lee, J. E. (2021). Reparative System Arising from CCR2(+) Monocyte Conversion Attenuates Neuroinflammation Following Ischemic Stroke. Translational Stroke Research. https://doi.org/10.1007/s12975-020-00878-x Cite
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