ArticleActa neuropathologica communications2024
Adequate post-ischemic reperfusion of the mouse brain requires endothelial NFAT5.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Surgical protocol and ischemic duration determine myeloid cell features and locomotor deficits in preclinical transient middle cerebral artery occlusion.Experimental neurology · 2026Article
- Erbin Confers Neuroprotection against Cerebral Ischemia-Reperfusion Injury in Mice via MAPK Pathway Inhibition.eNeuro · 2026Article
- Splicing-based biomarkers define a robust multigene classifier for relapsing-remitting multiple sclerosis.Journal of translational autoimmunity · 2025Article
- Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke.Genes & diseases · 2025Article
- Bidirectional Role of Pericytes in Ischemic Stroke.Brain sciences · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Severity and outcome of strokes following cerebral hypoperfusion are significantly influenced by stress responses of the blood vessels. In this context, brain endothelial cells (BEC) regulate inflammation, angiogenesis and the vascular resistance to rapidly restore perfusion. Despite the relevance of these responses for infarct volume and tissue recovery, their transcriptional control in BEC is not well characterized. We revealed that oxygen and nutrient-deprived BEC activate nuclear factor of activated T-cells 5 (NFAT5)-a transcription factor that adjusts the cellular transcriptome to cope with environmental stressors. We hypothesized that NFAT5 controls the expression of genes regulating the response of BEC in the ischemic brain. The functional relevance of NFAT5 was assessed in mice, allowing the conditional EC-specific knock-out of Nfat5 (Nfat5
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.