ArticleHuman molecular genetics2023
An altered extracellular matrix-integrin interface contributes to Huntington's disease-associated CNS dysfunction in glial and vascular cells.
Article in Human molecular genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Extracellular matrix remodeling therapeutic strategies to tackle central nervous system diseases.Neural regeneration research · 2026Article
- Comparative Genomic Screening Identifies Developmental Constraint Loci Underscoring the Phenotypic Evolution of Syngnathids.Integrative zoology · 2026Article
- Friend or foe? Glial-vascular interactions in health and neurodegenerative disease.Pharmacological reviews · 2026Review
- Role of Oxidative Stress in Human Neurodegenerative Pathologies: Lessons from theCurrent topics in medicinal chemistry · 2026Review
- Review
- cAMP/PKA signaling regulates TDP-43 aggregation and mislocalization.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Stem cell engineering approaches for investigating glial cues in central nervous system disorders.Current opinion in biotechnology · 2024Review
- Revolutionizing Ischemic Stroke Diagnosis and Treatment: The Promising Role of Neurovascular Unit-Derived Extracellular Vesicles.Biomolecules · 2024Review
- Mutant huntingtin confers cell-autonomous phenotypes on Huntington's disease iPSC-derived microglia.Scientific reports · 2023Article
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
Astrocytes and brain endothelial cells are components of the neurovascular unit that comprises the blood-brain barrier (BBB) and their dysfunction contributes to pathogenesis in Huntington's disease (HD). Defining the contribution of these cells to disease can inform cell-type-specific effects and uncover new disease-modifying therapeutic targets. These cells express integrin (ITG) adhesion receptors that anchor the cells to the extracellular matrix (ECM) to maintain the integrity of the BBB. We used HD patient-derived induced pluripotent stem cell (iPSC) modeling to study the ECM-ITG interface in astrocytes and brain microvascular endothelial cells and found ECM-ITG dysregulation in human iPSC-derived cells that may contribute to the dysfunction of the BBB in HD. This disruption has functional consequences since reducing ITG expression in glia in an HD Drosophila model suppressed disease-associated CNS dysfunction. Since ITGs can be targeted therapeutically and manipulating ITG signaling prevents neurodegeneration in other diseases, defining the role of ITGs in HD may provide a novel strategy of intervention to slow CNS pathophysiology to treat HD.
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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.