ArticleFrontiers in cellular neuroscience2019
TMEM16A Inhibition Preserves Blood-Brain Barrier Integrity After Ischemic Stroke.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- LRRC8A in endothelial cells contributes to the aberrant blood-brain barrier integrity in ischaemic stroke.Stroke and vascular neurology · 2025Article
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- Aging, vascular dysfunction, and the blood-brain barrier: unveiling the pathophysiology of stroke in older adults.Biogerontology · 2025Review
- Tamsulosin ameliorates bone loss by inhibiting the release of ClProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The emerging role of anoctamin-1 in cardiac and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Electromechanical Regulation Underlying Protein Nanoparticle-Induced Osmotic Pressure in Neurotoxic Edema.International journal of nanomedicine · 2025Article
- CaInternational journal of molecular sciences · 2024Review
- Multiomic approaches to stroke: the beginning of a journey.Nature reviews. Neurology · 2024Article
- Novel insight into the etiology of ischemic stroke gained by integrative multiome-wide association study.Human molecular genetics · 2024Article
- Protein nanoparticles induce the activation of voltage-dependent non-selective ion channels to modulate biological osmotic pressure in cytotoxic cerebral edema.Frontiers in pharmacology · 2024Article
- Novel insight into the etiology of ischemic stroke gained by integrative transcriptome-wide association study.medRxiv : the preprint server for health sciences · 2023Article
- Optogenetic Stimulation of mPFC Alleviates White Matter Injury-Related Cognitive Decline after Chronic Ischemia through Adaptive Myelination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Pharmacological modulation of chloride channels as a therapeutic strategy for neurological disorders.Frontiers in physiology · 2023Review
- Arctigenin Attenuates Vascular Inflammation Induced by High Salt through TMEM16A/ESM1/VCAM-1 Pathway.Biomedicines · 2022Article
- The Ca2+-gated channel TMEM16A amplifies capillary pericyte contraction and reduces cerebral blood flow after ischemia.The Journal of clinical investigation · 2022Article
- A monoamine oxidase B inhibitor ethyl ferulate suppresses microglia-mediated neuroinflammation and alleviates ischemic brain injury.Frontiers in pharmacology · 2022Article
- TMEM16A Plays an Insignificant Role in Myocardium Remodeling but May Promote Angiogenesis of Heart During Pressure-overload.Frontiers in physiology · 2022Article
- The Novel lncRNA ENST00000530525 Affects ANO1, Contributing to Blood-Brain Barrier Injury in Cultured hCMEC/D3 Cells Under OGD/R Conditions.Frontiers in genetics · 2022Article
- Silencing of lncRNA XIST impairs angiogenesis and exacerbates cerebral vascular injury after ischemic stroke.Molecular therapy. Nucleic acids · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammatory response plays a pivotal role in Blood-Brain Barrier (BBB) destruction following ischemic brain injury. Enhanced leukocyte adhesion to vascular endothelial cells is an essential event in the inflammatory process. TMEM16A, a newly discovered protein regulating calcium-activated chloride channels, is widely expressed in eukaryotes. Recent studies have suggested that upregulated expression of TMEM16A is associated with the occurrence and development of many diseases. However, the role of TMEM16A in regulating BBB integrity after ischemic stroke has not been fully investigated. In this study, we found that TMEM16A is mainly expressed in brain endothelial cells and upregulated after ischemic stroke in the mouse brain. Caccinh-A01, an TMEM16A inhibitor that reduced its upregulation, attenuated brain infarct size and neurological deficits after ischemic stroke. ICAM-1 and MPO expression and BBB permeability were decreased after TMEM16A inhibitor administration. In addition, TMEM16A silencing rescued oxygen-glucose deprivation/reoxygenation (OGD/R)-induced transendothelial permeability
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