ArticleThe Journal of clinical investigation2023
TMEM16E regulates endothelial cell procoagulant activity and thrombosis.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2027Review
- TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Adenosine receptor signaling in vascular diseases: from molecular mechanisms to targeted therapeutics.Acta pharmacologica Sinica · 2026Review
- RAP1-RHO small GTPase cross-talk mediates integrindependent and -independent platelet procoagulant response.Haematologica · 2026Article
- Volume electron microscopy reveals heterogeneity of the hemostatic response in veins and arteries.Blood advances · 2026Article
- Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.Cell communication and signaling : CCS · 2026Review
- In vivo targeting of open prothrombin with the monoclonal antibody POmAb results in anticoagulation without excessive bleeding.Journal of thrombosis and haemostasis : JTH · 2026Article
- Comprehensive analysis of efferocytosis-related genes in diagnosis and immune infiltration in atherosclerosis: based on bulk and single-cell RNA sequencing data.Frontiers in cell and developmental biology · 2026Article
- A bismuth-based nanoplatform with synergistic fibrin/NET disruption and antioxidant/anti-inflammatory capabilities for enhanced thrombolysis and prevention of deep vein thrombosis recurrence.Journal of nanobiotechnology · 2025Article
- Investigation of Antithrombotic Activity and In Vivo Effective Forms of Kaempferitrin Using FeClMolecules (Basel, Switzerland) · 2025Article
- Endo-chip laser-induced thrombus formation: a vessel-on-chip model for in vitro testing of antithrombotic agents.Blood vessels, thrombosis & hemostasis · 2025Article
- Overlapping risk factors and pathogenic mechanisms in lung cancer and cardiovascular disease.Discover oncology · 2025Review
- Endothelial Trauma Depends on Surface Charge and Extracellular Calcium Levels.bioRxiv : the preprint server for biology · 2025Article
- Apoptotic cells promote circulating tumor cell survival and metastasis.Communications biology · 2025Article
- Mechanical Biomimetic Nanocomposites for Multidimensional Treatment of Arterial Thrombosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Endothelial cell activation enhances thromboinflammation in vaccine-induced immune thrombotic thrombocytopenia.Blood advances · 2025Article
- Inpatient Outcomes for Patients With Peripheral Artery Disease Hospitalized for Acute Myocardial Infarction.Journal of the American Heart Association · 2025Article
- Transmembrane thiol isomerase TMX1 inhibits fibrin formation by down-regulation of platelet phosphatidylserine exposure.Cell communication and signaling : CCS · 2025Article
- ENDOTHELIAL-SPECIFIC KNOCKOUT OF THE SCRAMBLASE TMEM16F IMPAIRS IN VIVO CLOT FORMATION.Shock (Augusta, Ga.) · 2025Article
- Phosphatidylserine-blocking nanoparticles inhibit thrombosis without increased bleeding in mice.Journal of thrombosis and haemostasis : JTH · 2025Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Endothelial cells (ECs) normally form an anticoagulant surface under physiological conditions, but switch to support coagulation following pathogenic stimuli. This switch promotes thrombotic cardiovascular disease. To generate thrombin at physiologic rates, coagulation proteins assemble on a membrane containing anionic phospholipid, most notably phosphatidylserine (PS). PS can be rapidly externalized to the outer cell membrane leaflet by phospholipid "scramblases," such as TMEM16F. TMEM16F-dependent PS externalization is well characterized in platelets. In contrast, how ECs externalize phospholipids to support coagulation is not understood. We employed a focused genetic screen to evaluate the contribution of transmembrane phospholipid transport on EC procoagulant activity. We identified 2 TMEM16 family members, TMEM16F and its closest paralog, TMEM16E, which were both required to support coagulation on ECs via PS externalization. Applying an intravital laser-injury model of thrombosis, we observed, unexpectedly, that PS externalization was concentrated at the vessel wall, not on platelets. TMEM16E-null mice demonstrated reduced vessel-wall-dependent fibrin formation. The TMEM16 inhibitor benzbromarone prevented PS externalization and EC procoagulant activity and protected mice from thrombosis without increasing bleeding following tail transection. These findings indicate the activated endothelial surface is a source of procoagulant phospholipid contributing to thrombus formation. TMEM16 phospholipid scramblases may be a therapeutic target for thrombotic cardiovascular disease.
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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.