ArticleNeuron2022
Neuroinflammatory disease disrupts the blood-CNS barrier via crosstalk between proinflammatory and endothelial-to-mesenchymal-transition signaling.
Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
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- COVID-19 and Radiological Progression of Multiple Sclerosis.Diagnostics (Basel, Switzerland) · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Neuronal guidance signaling in neurodegenerative diseases: Key regulators that function at neuron-glia and neuroimmune interfaces.Neural regeneration research · 2026Article
- The small GTPase ARF6 regulates sphingolipid homeostasis and supports proliferation in acute myeloid leukemia.Haematologica · 2026Article
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Navigation Between Alzheimer's Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology-Genetics and Neuroinflammation.International journal of molecular sciences · 2025Review
- Article
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- Strategies for delivering drugs across the blood-brain barrier for the treatment of neurodegenerative diseases.Frontiers in drug delivery · 2025Review
- Organelle stresses and energetic metabolisms promote endothelial-to-mesenchymal transition and fibrosis via upregulating FOSB and MEOX1 in Alzheimer's disease.Frontiers in molecular neuroscience · 2025Article
- Single-cell transcriptome unveils unique transcriptomic signatures of human organ-specific endothelial cells.Basic research in cardiology · 2024Article
- Glia dysfunction in schizophrenia: evidence of possible therapeutic effects of nervonic acid in a preclinical model.Psychopharmacology · 2024Article
- Spatial correspondence among regional gene expressions and gray matter volume loss in multiple sclerosis.Molecular psychiatry · 2024Article
- Biomimetic Self-Propelled Asymmetric Nanomotors for Cascade-Targeted Treatment of Neurological Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Endothelial-Specific Reduction in Arf6 Impairs Insulin-Stimulated Vasodilation and Skeletal Muscle Blood Flow Resulting in Systemic Insulin Resistance in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Brain organoid as a model to study the role of mitochondria in neurodevelopmental disorders: achievements and weaknesses.Frontiers in cellular neuroscience · 2024Review
- Cerebral Cavernous Malformation (CCM)-like Vessel Lesion in the AgedExperimental neurobiology · 2023Article
- ADP-Ribosylation Factor 6 Pathway Acts as a Key Executor of Mesenchymal Tumor Plasticity.International journal of molecular sciences · 2023Review
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Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
Abstract
Breakdown of the blood-central nervous system barrier (BCNSB) is a hallmark of many neuroinflammatory disorders, such as multiple sclerosis (MS). Using a mouse model of MS, experimental autoimmune encephalomyelitis (EAE), we show that endothelial-to-mesenchymal transition (EndoMT) occurs in the CNS before the onset of clinical symptoms and plays a major role in the breakdown of BCNSB function. EndoMT can be induced by an IL-1β-stimulated signaling pathway in which activation of the small GTPase ADP ribosylation factor 6 (ARF6) leads to crosstalk with the activin receptor-like kinase (ALK)-SMAD1/5 pathway. Inhibiting the activation of ARF6 both prevents and reverses EndoMT, stabilizes BCNSB function, reduces demyelination, and attenuates symptoms even after the establishment of severe EAE, without immunocompromising the host. Pan-inhibition of ALKs also reduces disease severity in the EAE model. Therefore, multiple components of the IL-1β-ARF6-ALK-SMAD1/5 pathway could be targeted for the treatment of a variety of neuroinflammatory disorders.
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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 OpenQuestion graph.