ArticleJournal of neuroinflammation2020
KLF4 alleviates cerebral vascular injury by ameliorating vascular endothelial inflammation and regulating tight junction protein expression following ischemic stroke.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 62 citations in OpenAlex.
- Effect of Stroke Severity on Efficacy and Safety of Indobufen versus Aspirin in Patients with Moderate to Severe Stroke: Results from the INSURE Randomized Clinical Trial.Journal of atherosclerosis and thrombosis · 2025Trial
- The regulatory network of Mfsd2a in cerebral ischemia: a novel time-targeted intervention framework.Molecular biology reports · 2026Review
- Total Flavonoids from Snow Chrysanthemum Exert Synergistic Vascular and Neuroprotective Effects in Hypertensive Vascular Dementia Rats.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- Pervasive neurovascular dysfunction in the ventromedial prefrontal cortex of female depressed suicides with a history of childhood abuse.Molecular psychiatry · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Simultaneously infer cell pseudotime, velocity field, and gene interaction from multi-branch scRNA-seq data with scPN.NAR genomics and bioinformatics · 2025Article
- mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025Review
- MiR-7a-Klf4 axis as a regulator and therapeutic target of neuroinflammation and ferroptosis in Alzheimer's disease.NAR molecular medicine · 2025Article
- hUC-MSC extracellular vesicles protect against hypoxic-ischemic brain injury by promoting NLRP3 ubiquitination.Biomolecules & biomedicine · 2025Article
- Krüppel-like factor 4 transcription factor in blood-brain barrier endothelial cells: A potential role in Alzheimer's disease.Animal models and experimental medicine · 2025Review
- Alterations of circulating exosomal microRNAs in an LPS-induced depression model of male mice: Potential role in the anti-depressive effects of acupuncture.Physiological reports · 2025Article
- Identification of Cell Fate Determining Transcription Factors for Generating Brain Endothelial Cells.Stem cell reviews and reports · 2025Article
- Mechanism of disturbed endothelial cell function on angiogenesis following ischemic brain stroke (Review).Experimental and therapeutic medicine · 2025Review
- Identification of key genes associated with oxidative stress in ischemic stroke via bioinformatics integrated analysis.BMC neuroscience · 2025Article
- Advances in the detection of biomarkers for ischemic stroke.Frontiers in neurology · 2025Review
- Single-cell sequencing reveals the response mechanisms of vascular endothelial cells to glucocorticoids in diabetic retinopathy.PloS one · 2025Article
- Exploring the Functionality of the Krüppel-like Factors in Kidney Development, Metabolism, and Diseases.Life (Basel, Switzerland) · 2024Review
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Authors and funding
7 authors at 5 institutions in 1 country.
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Abstract
backgroundAlthough inflammatory cell adhesion molecules (CAMs) and anti-inflammation factor Kruppel-like transcription factor (KLF) 4 have all been reported to be induced after cerebral ischemic stroke (CIS), the close temporal and spatial relationship between expressions of CAMs and KLF4 following CIS and whether and how CAMs and KLF-4 contribute to the development of CIS-induced vascular injury are still unclear.
methodsHere, we first examined the correlation between serum levels of CAMs/KLF4 and infarct volume in acute CIS patients. Then, we determined the relationship between CAMs and KLF4 in mice after focal cerebral ischemia. Finally, we investigated the mechanism of KLF4 in protecting against oxygen-glucose deprivation-induced brain endothelial cell injury.
resultsOur results demonstrated that patients with moderate to severe CIS had higher serum levels of three CAMs including E-selectin, inter-cellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) but lower levels of KLF4 at 48 h after an acute event as compared to patients with minor CIS. The expression levels of three CAMs as well as KLF4 all correlated well with the infarct volume in all the CIS subjects at that time. Although the expressions of three CAMs and KLF4 were all induced in the ischemic hemisphere following focal cerebral ischemia, the peak timing and distribution patterns of their expression were different: the induction of KLF4 lagged behind that of the CAMs in the ischemic penumbra; furthermore, the dual immunofluorescent studies displayed that high expression of KLF4 was always associated with relatively less cerebral vascular endothelial inflammation response in the ischemic hemisphere and vice versa. Mechanistic analyses revealed that KLF4 alleviated CIS-induced cerebral vascular injury by regulating endothelial expressions of CAMs, nuclear factor-kB, and tight junction proteins.
conclusionsThese data indicate that KLF4 confers vascular protection against cerebral ischemic injury, suggesting that circulating CAMs and KLF4 might be used as potential biomarkers for predicting the prognosis of acute ischemic stroke and also providing a new proof of concept and potential targets for future prevention and treatment of CIS.
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