ArticleJournal of the American Heart Association2026
Loss of Endothelial YAP/TAZ Reduces the Size of Chronic Stroke Lesions and Alters the Endothelial Environment.
Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Endothelial Yes-Associated Protein/Transcription Regulator 1: From Angiogenic Driver to Poststroke Immune Gatekeeper.Journal of the American Heart Association · 2026Article
- Unmasking the Hidden Burden: Inflammation and Cardiovascular DiseaseJournal of the American Heart Association · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic stroke remains a leading cause of morbidity and mortality worldwide, with limited treatment options available. Vascular dysfunction is a key pathomechanism, and brain endothelial cells (bECs) play a critical role in determining stroke outcomes. This study investigates the specific roles of YAP (yes-associated protein 1) and TAZ (WW domain containing transcription regulator 1) in regulating bEC functions during stroke.
methodsMice underwent 30-minute middle cerebral artery occlusion (MCAo) followed by reperfusion to model ischemic stroke. TAZ reporter mice were used to track stroke-induced subcellular changes in TAZ expression. Tamoxifen-inducible endothelial-specific
resultsMiddle cerebral artery occlusion/reperfusion regulated
conclusionsOur data suggest that endothelial YAP/TAZ affects the inflammatory milieu subacutely after ischemia and thereby influences the chronic course of stroke. Modulation of YAP/TAZ activity in ECs may be a promising therapeutic target to promote neuroprotection after stroke.
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