ArticleBlood2024
Deciphering and disrupting PIEZO1-TMEM16F interplay in hereditary xerocytosis.
Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 29 citations in OpenAlex.
- 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
- Piezo1 in Peripheral and Central Sensitisation: Implications for Chronic Pain.Bioengineering (Basel, Switzerland) · 2026Review
- Mechanisms of Piezo1-Mediated Mechanotransduction in Thrombotic Diseases.International journal of molecular sciences · 2026Review
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2026Review
- Piezo1 channel: structure, mechanogating mechanism, functions, diseases and therapeutic strategy.Molecular biomedicine · 2026Review
- PIEZO1 is Required for Acute Myeloid Leukemia Progression and Leukemia Stem Cell Maintenance via HIF1A-SLC7A11 Axis-Mediated Ferroptosis Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RAP1-RHO small GTPase cross-talk mediates integrindependent and -independent platelet procoagulant response.Haematologica · 2026Article
- The extracellular matrix Piezo1 feedback loop drives renal fibrosis through compartment-specific mechanotransduction.International urology and nephrology · 2026Review
- Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.Cell communication and signaling : CCS · 2026Review
- Lipid Regulation of Mechanosensitive Ion Channels.International journal of molecular sciences · 2026Review
- Piezo1 Mechanosensor Expression in Rare Hematopoietic Cells Controls Systemic Inflammatory Response in Mice.Cells · 2025Article
- Molecular surprises in evaluations of red cell disorders.Hematology. American Society of Hematology. Education Program · 2025Review
- Mechanotransduction mechanisms in human erythrocytes: Fundamental physiology and clinical significance.Channels (Austin, Tex.) · 2025Review
- Targeting PIEZO1-TMEM16F Coupling to Mitigate Sickle Cell Disease Complications.American journal of hematology · 2025Article
- PIEZO1 gain-of-function mutation drives cardiomyopathy by disrupting myocardial lipid homeostasis besides iron overload.Science advances · 2025Article
- Clinical and Genetic Analysis of Dehydrated Hereditary Stomatocytosis: A Case Report.Clinical case reports · 2025Article
- Activation of WNK1 signaling through Piezo1.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PIEZO1 drives trophoblast fusion and placental development.Nature communications · 2025Article
- Progress and challenges in the development of clinically viable Piezo1 inhibitors.Future medicinal chemistry · 2025Article
- RBC-GEM: A genome-scale metabolic model for systems biology of the human red blood cell.PLoS computational biology · 2025Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
abstractCell-surface exposure of phosphatidylserine (PS) is essential for phagocytic clearance and blood clotting. Although a calcium-activated phospholipid scramblase (CaPLSase) has long been proposed to mediate PS exposure in red blood cells (RBCs), its identity, activation mechanism, and role in RBC biology and disease remain elusive. Here, we demonstrate that TMEM16F, the long-sought-after RBC CaPLSase, is activated by calcium influx through the mechanosensitive channel PIEZO1 in RBCs. PIEZO1-TMEM16F functional coupling is enhanced in RBCs from individuals with hereditary xerocytosis (HX), an RBC disorder caused by PIEZO1 gain-of-function channelopathy. Enhanced PIEZO1-TMEM16F coupling leads to an increased propensity to expose PS, which may serve as a key risk factor for HX clinical manifestations including anemia, splenomegaly, and postsplenectomy thrombosis. Spider toxin GsMTx-4 and antigout medication benzbromarone inhibit PIEZO1, preventing force-induced echinocytosis, hemolysis, and PS exposure in HX RBCs. Our study thus reveals an activation mechanism of TMEM16F CaPLSase and its pathophysiological function in HX, providing insights into potential treatment.
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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.