ArticleNature communications2026
Anisodine hydrobromide targets matk and prevents delayed rtPA thrombolysis-induced vasogenic cerebral edema in ischemic stroke.
Article in Nature communications, 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.
- Derivatization-Assisted Lipase-Mediated Separation of Optically Pure α-Cyclopentylmandelic Acid Through Enhanced Substrate Recognition.Molecules (Basel, Switzerland) · 2026Article
- Anisodine hydrobromide targets matk and prevents delayed rtPA thrombolysis-induced vasogenic cerebral edema in ischemic stroke.Nature communications · 2026Article
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Authors and funding
11 authors.
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Abstract
Vasogenic cerebral edema is a severe complication of delayed thrombolysis for ischemic stroke, for which no pharmacological treatment exists. Anisodine hydrobromide (Ani), an alkaloid used clinically in China for vascular disorders, is investigated for its potential to mitigate this condition. Here we show that Ani treatment improves survival and neurological function in a mouse model of delayed rtPA-induced cerebral edema by preserving the integrity of the blood-brain barrier. Utilizing proteomics and microarray screening, we identify megakaryocyte-associated tyrosine kinase (Matk) as a direct target of Ani. We demonstrate that Ani binding stabilizes Matk, preventing its degradation and suppressing the activation of Src kinase. This inhibition consequently blocks the dual paracellular and transcellular leakage pathways that drive vasogenic edema. Our findings reveal the Matk-Src signaling axis as a therapeutic target and support Ani as a promising clinical candidate for preventing post-thrombolytic complications in stroke management.
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Registered trials
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