ArticleNature communications2025
Endothelial SHANK3 regulates tight junctions in the neonatal mouse blood-brain barrier through β-Catenin signaling.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Convergent blood-brain barrier breakdown in schizophrenia and autism spectrum disorders: a systematic review of preclinical animal models.Fluids and barriers of the CNS · 2026Pooled it
- Neutrophil-mediated BDNF delivery for the treatment of moderate to severe Alzheimer's disease.Acta pharmaceutica Sinica. B · 2026Article
- Targeted Retention of Cationic Liposomes at the Inflamed Blood-Brain Barrier by Incorporating Mesenchymal Stem Cell Membrane.Advanced healthcare materials · 2026Article
- Inflammation increases the penetrance of behavioral impairment in Shank3 haploinsufficiency mice - can it explain the behavioral regression in Autism?Molecular psychiatry · 2026Article
- Modulation of Homer1 EVH1 domain internal dynamics by putative autism-associated mutations.FEBS letters · 2026Article
- Reduced BCL2 level in astrocytes contributes to blood-brain barrier disruption in the striatum of offspring exposed to maternal preeclampsia.Molecular psychiatry · 2026Article
- Shank3 related oligodendrocyte alterations in autism are restored by Erk pathway inhibition.Molecular psychiatry · 2026Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- RIPK1 kinase drove brain microvascular endothelial cells death and blood-brain barrier disruption in neonatal Escherichia coli meningitis.Nature communications · 2025Article
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
- Mesenchymal Stem Cells Restore Endothelial Integrity and Alleviate Emotional Impairments in a Diabetic Mouse Model via Inhibition of MMP-9 Activity.International journal of molecular sciences · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disability condition arising from a combination of genetic and environmental factors. Despite the blood-brain barrier (BBB) serving as a crucial gatekeeper, conveying environmental influences into the brain parenchyma, the contributions of BBB in ASD pathogenesis remain largely uncharted. Here we report that SHANK3, an ASD-risk gene, expresses in the BBB-forming brain endothelial cells (BECs) and regulates tight junctional (TJ) integrity essential for BBB's barrier function. Endothelium-specific Shank3 (eShank3) knockout (KO) neonatal mice exhibit male-specific BBB-hyperpermeability, reduced neuronal excitability, and impaired ultra-sonic communications. Although BBB permeability is restored during adult age, the male mutant mice display reduced neuronal excitability and impaired sociability. Further analysis reveals that the BBB-hyperpermeability is attributed to the β-Catenin imbalance triggered by eShank3-KO. These findings highlight a pathogenic mechanism stemming from the ASD-risk Shank3, emphasizing the significance of neonatal BECs in the BBB as a potential therapeutic target for ASD.
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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.