ArticleJournal of advanced research2026
Astrocyte-derived LAMC1 protects against intracerebral hemorrhage: A novel genetic mechanism maintaining neurovascular integrity.
Article in Journal of advanced research, 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.
- Berberine targets the PI3Kα LYS672 site to suppress the PI3K/Akt/NF-κB axis and modulate microglial functional states after intracerebral hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Astrocyte-blood-brain barrier crosstalk in cerebral small vessel disease: linking barrier dysfunction to neurovascular failure.Frontiers in neurology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIntracerebral hemorrhage (ICH) is a devastating stroke subtype, yet the intrinsic mechanisms conferring genetic protection against it remain poorly understood. While risk-associated loci have been identified, the cell-type-specific pathways that actively preserve cerebrovascular stability remain largely unmapped.
objectivesThis study aimed to bridge the critical gap in understanding cell-type-specific mechanisms of ICH by identifying novel protective genetic drivers essential for maintaining neurovascular integrity, utilizing an integrative multi-omics approach.
methodsWe integrated large-scale human genetic data with multi-omics approaches (TWAS, PWAS) and single-cell analysis to identify cell-type-specific risk genes for ICH. We validated our core findings using a collagenase-induced mouse model of ICH. To definitively establish causality, we further conducted in vivo gain-of-function studies via retro-orbital injection of adeno-associated virus (AAV) vectors. By combining Evans Blue extravasation assays, brain edema measurements, and neurobehavioral testing, we systematically evaluated the impact of LAMC1 on blood-brain barrier (BBB) integrity and neurological functional outcomes.
resultsMulti-omics analysis indicated that genetically determined reduced LAMC1 expression increases ICH risk, with single-cell eQTL pinpointing astrocytes as key drivers. In vivo, LAMC1 was downregulated in astrocytes and endothelial cells post-ICH. Crucially, LAMC1 overexpression attenuated brain edema and tissue necrosis, markedly improving neuromotor function. Mechanistically, LAMC1 preserved BBB integrity by inhibiting the degradation of the tight junction proteins ZO-1 and occludin.
conclusionThis study not only identifies astrocyte-derived LAMC1 as a "vascular guardian" essential for maintaining neurovascular unit integrity, but also provides definitive causal evidence via gain-of-function experiments that elevating LAMC1 levels effectively stabilizes the blood-brain barrier and improves ICH outcomes. Consequently, this establishes LAMC1 as a critical target for precision intervention aimed at enhancing vascular resilience and for the prevention and treatment of ICH.
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