ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2019
PDGFR-β restores blood-brain barrier functions in a mouse model of focal cerebral ischemia.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The trial behind it
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Who cites it
65 citing papers in PubMed, 104 citations in OpenAlex.
- KLF2 Is Associated with ERK1/2-MAP2 Activation and Neuron-like Phenotypic Remodeling of PDGFR-β-Lineage Cells Following Ischemic Stroke.Brain sciences · 2026Article
- Gut bacterial metabolite imidazole propionate potentiates Alzheimer's disease pathology.Nature communications · 2026Article
- Central nervous system pericytes express soluble ST2 in inflammation and injury.Molecular brain · 2026Article
- Spatiotemporal dynamics of brain pericytes in ischemic stroke.Journal of neuroinflammation · 2026Review
- NOTCH3 Mutations in CADASIL: a multicellular perspective on neurodegeneration.Cell communication and signaling : CCS · 2026Review
- Modulation of the Receptor Tyrosine Kinase TIE2/International journal of molecular sciences · 2026Article
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- Brain pericytes derived from human pluripotent stem cells retain vascular and phagocytic functions under hypoxia.Stem cells (Dayton, Ohio) · 2025Article
- Imatinib prevents blood-spinal cord barrier disruption by inhibiting PDGFR-mediated JMJD3 expression and activation after spinal cord injury.Fluids and barriers of the CNS · 2025Article
- Bidirectional Role of Pericytes in Ischemic Stroke.Brain sciences · 2025Review
- Interplay Between Vascular Dysfunction and Neurodegenerative Pathology: New Insights into Molecular Mechanisms and Management.Biomolecules · 2025Review
- A molecular brain atlas reveals cellular shifts during the repair phase of stroke.Journal of neuroinflammation · 2025Article
- Imatinib on target in stroke recovery.The Journal of clinical investigation · 2025Article
- Contribution of brain pericytes to neuroinflammation following repetitive head trauma.Journal of inflammation (London, England) · 2025Article
- Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.Frontiers in physiology · 2025Article
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
- The Possible Mechanistic Basis of Individual Susceptibility to Spike Protein Injury.Advances in virology · 2025Review
- Zi Shen Wan Fang repaired blood-brain barrier integrity in diabetic cognitive impairment mice via preventing cerebrovascular cells senescence.Chinese medicine · 2024Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although platelet-derived growth factor receptor beta (PDGFR-β) mediates the recruitment of vascular pericytes into ischemic lesion to restore the blood-brain barrier (BBB) dysfunction, its mechanisms still remain elusive
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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.