ArticleCell death & disease2022
Endothelial ETS1 inhibition exacerbate blood-brain barrier dysfunction in multiple sclerosis through inducing endothelial-to-mesenchymal transition.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
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- Spatially resolved multiomics of human meningeal development reveal lineage and disease dynamics.Nature cell biology · 2026Article
- The Roles of Transcription Factor Ets-1 in Neurological Disorders.Molecular neurobiology · 2026Review
- Multiancestry genome-wide association and multiomics analyses elucidate spatiocellular features of multiple sclerosis genetics.Nature genetics · 2026Article
- Engineered ETS1-Nanoconjugate Restores Immune Homeostasis through Dual Immune-Vascular Modulation in Relapsing and Progressive Multiple Sclerosis.Advanced healthcare materials · 2026Article
- Vascular and Neural Transcriptomics Reveal Stage-Dependent Pathways to Inflammation and Cognitive Dysfunction in a Rat Model of Hypertension.Journal of the American Heart Association · 2026Article
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Trametinib Decreased Intracerebral Hemorrhages and Endothelial-to-Mesenchymal Transition in KRASStroke · 2026Article
- Microvascular endothelial metabolic dysfunction drives cerebral edema through bioenergetic failure after ischemia-reperfusion.Theranostics · 2026Article
- Smoldering neuroinflammation in progressive multiple sclerosis: mechanisms, imaging biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Gut microbes-spinal connection is required for itch sensation.Gut microbes · 2025Article
- Gut microbiota modulates CNS barrier function in murine model for multiple sclerosis.Fluids and barriers of the CNS · 2025Article
- 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
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- Therapeutic limitations of oncolytic VSVd51-mediated miR-199a-5p delivery in triple negative breast cancer models.Scientific reports · 2025Article
- Sex Hormone-Related Pathogenic Genes in Multiple Sclerosis: A Multi-omics Mendelian Randomization Study.Journal of molecular neuroscience : MN · 2025Article
- Embryonic 6:2 Fluorotelomer Alcohol Exposure Disrupts the Blood‒Brain Barrier by Causing Endothelial‒to‒Mesenchymal Transition in the Male Mice.Molecular neurobiology · 2025Article
- In silico screening system based on a transcription factors regulatory network only using transcriptomic data.PloS one · 2025Article
- Single-Cell RNA Sequencing Uncovers Pathological Processes and Crucial Targets for Vascular Endothelial Injury in Diabetic Hearts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood-brain barrier (BBB) dysfunction has been recognized as an early pathological feature and contributing factor in multiple sclerosis. Endothelial-to-mesenchymal transition is a process associated with endothelial dysfunction leading to the disruption of vessel stability and barrier function, yet its functional consequence in multiple sclerosis remains unclear. Here, we demonstrated that endothelial-to-mesenchymal transition accompanied the blood-brain barrier dysfunction in several neurological disorders, especially in multiple sclerosis. The activity of transcription factor ETS1, which is highly expressed in endothelial cells (ECs) and responded to an inflammatory condition, is suppressed in the central nervous system (CNS) ECs in MS and its animal model experimental autoimmune encephalomyelitis. We identify ETS1 as a central regulator of endothelial-to-mesenchymal transition (EndMT) associated with the compromise of barrier integrity. These phenotypical and functional alterations can further induce high permeability, immune infiltration, and organ fibrosis in multiple sclerosis, thus promoting disease progression. Together, these results demonstrate a functional role of EndMT in blood-brain barrier dysfunction and propose ETS1 as a potential transcriptional switch of EndMT to target the development of multiple sclerosis.
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