ArticleProceedings of the National Academy of Sciences of the United States of America2025
Enhanced PIEZO1 function contributes to the pathogenesis of sickle cell disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Deoxy-Piezo1 hyperactivity elevates pump-leak fluxes and lactate production in sickle cells.Biophysical journal · 2026Article
- PIEZO1-mediated mechanosensation links aging to bladder dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Yoda molecules agonize PIEZO2.bioRxiv : the preprint server for biology · 2026Article
- Lipid Regulation of Mechanosensitive Ion Channels.International journal of molecular sciences · 2026Review
- Targeting PIEZO1-TMEM16F Coupling to Mitigate Sickle Cell Disease Complications.American journal of hematology · 2025Article
- Enhanced PIEZO1 function contributes to the pathogenesis of sickle cell disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Abstract
Sickle cell disease (SCD), an inherited blood disorder caused by a mutation in the β-globin gene, is characterized by sickle erythrocytes that are prone to hemolysis, leading to anemia and vaso-occlusion crises. In sickle erythrocytes, hemoglobin aggregation is followed by altered cation permeability and subsequent dehydration. Interventions that restore cation permeability can decrease hemolysis and ameliorate the symptoms associated with SCD. PIEZO1 is a nonselective mechanosensitive cation channel that regulates erythrocyte volume. Gain-of-function (GOF) mutations in PIEZO1 cause hemolytic anemia by increasing cation permeability, leading to erythrocyte dehydration in humans and mice. Although PIEZO1 plays a key role in erythrocyte homeostasis, its role in SCD remains unknown. Here, we demonstrate that the function of the PIEZO1 channel is upregulated in sickle erythrocytes of humans and mice, and this enhancement can be restored through a dietary intervention. We found that PIEZO1 activity in sickle erythrocytes resembles that of the GOF mutation causing hemolytic anemia. A diet enriched in the
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