ArticleBrain : a journal of neurology2013
KLF11 mediates PPARγ cerebrovascular protection in ischaemic stroke.
Article in Brain : a journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 107 citations in OpenAlex.
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- Nitro-oleic acid activation of endothelial PPARγ signaling pathway alleviates neurovascular injury and improves functional outcomes in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2026Article
- Genetic deletion of microRNA-15a/16-1 in pericytes stimulates cerebral angiogenesis and promotes functional recovery after ischemic stroke.Angiogenesis · 2025Article
- Clinical exome sequencing identifies novel gene variants associated with ischemic stroke in the Saudi Tabuk population.Frontiers in human neuroscience · 2025Article
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Endothelial KLF11 is a novel protector against diabetic atherosclerosis.Cardiovascular diabetology · 2024Article
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- Loss of microRNA-15a/16-1 function promotes neuropathological and functional recovery in experimental traumatic brain injury.JCI insight · 2024Article
- No-reflow after recanalization in ischemic stroke: From pathomechanisms to therapeutic strategies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- Hypoxia exposure blunts angiogenic signaling and upregulates the antioxidant system in endothelial cells derived from elephant seals.BMC biology · 2024Article
- [Upregulating KLF11 ameliorates intestinal inflammation in mice with 2, 4, 6-trinitrobenesulfonic acid-induced colitis by inhibiting the JAK2/STAT3 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- miR-10a-5p Regulates the Proliferation and Differentiation of Porcine Preadipocytes Targeting the KLF11 Gene.Animals : an open access journal from MDPI · 2024Article
- Genetic deletion of Krüppel-like factor 11 aggravates traumatic brain injury.Journal of neuroinflammation · 2022Article
- Endothelial KLF11 as a Nephroprotectant in AKI.Kidney360 · 2022Article
- Essential role of MALAT1 in reducing traumatic brain injury.Neural regeneration research · 2022Article
- KLF11 Protects against Venous Thrombosis via Suppressing Tissue Factor Expression.Thrombosis and haemostasis · 2022Article
- Nuclear Receptors in Myocardial and Cerebral Ischemia-Mechanisms of Action and Therapeutic Strategies.International journal of molecular sciences · 2021Review
- Current knowledge of Krüppel-like factor 5 and vascular remodeling: providing insights for therapeutic strategies.Journal of molecular cell biology · 2021Review
- KLF11 protects against abdominal aortic aneurysm through inhibition of endothelial cell dysfunction.JCI insight · 2021Article
- Spatially mapped single-cell chromatin accessibility.Nature communications · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptor gamma (PPARγ) is emerging as a major regulator in neurological diseases. However, the role of (PPARγ) and its co-regulators in cerebrovascular endothelial dysfunction after stroke is unclear. Here, we have demonstrated that (PPARγ) activation by pioglitazone significantly inhibited both oxygen-glucose deprivation-induced cerebral vascular endothelial cell death and middle cerebral artery occlusion-triggered cerebrovascular damage. Consistent with this finding, selective (PPARγ) genetic deletion in vascular endothelial cells resulted in increased cerebrovascular permeability and brain infarction in mice after focal ischaemia. Moreover, we screened for (PPARγ) co-regulators using a genome-wide and high-throughput co-activation system and revealed KLF11 as a novel (PPARγ) co-regulator, which interacted with (PPARγ) and regulated its function in mouse cerebral vascular endothelial cell cultures. Interestingly, KLF11 was also found as a direct transcriptional target of (PPARγ). Furthermore, KLF11 genetic deficiency effectively abolished pioglitazone cytoprotection in mouse cerebral vascular endothelial cell cultures after oxygen-glucose deprivation, as well as pioglitazone-mediated cerebrovascular protection in a mouse middle cerebral artery occlusion model. Mechanistically, we demonstrated that KLF11 enhanced (PPARγ) transcriptional suppression of the pro-apoptotic microRNA-15a (miR-15a) gene, resulting in endothelial protection in cerebral vascular endothelial cell cultures and cerebral microvasculature after ischaemic stimuli. Taken together, our data demonstrate that recruitment of KLF11 as a novel (PPARγ) co-regulator plays a critical role in the cerebrovascular protection after ischaemic insults. It is anticipated that elucidating the coordinated actions of KLF11 and (PPARγ) will provide new insights into understanding the molecular mechanisms underlying (PPARγ) function in the cerebral vasculature and help to develop a novel therapeutic strategy for the treatment of stroke.
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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.