ArticleeLife2025
Structure of human PIEZO1 and its slow-inactivating channelopathy mutants.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Piezo1-mediated Mechanotransduction in the musculoskeletal system: Signaling networks and therapeutic perspectives.Bone reports · 2026Review
- Piezo1 channel: structure, mechanogating mechanism, functions, diseases and therapeutic strategy.Molecular biomedicine · 2026Review
- Article
- A two-step clockwork mechanism opens a proteo-lipidic pore in PIEZO2.Nature chemical biology · 2026Article
- Lipid composition and mechanical force underlie multi-modal regulation of Piezo1 gating.Science advances · 2026Article
- MDFIC2 is a sensory neuron-specific PIEZO channel auxiliary subunit.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Lipid Regulation of Mechanosensitive Ion Channels.International journal of molecular sciences · 2026Review
- Structures of invertebrate PEZO-1 isoforms with a compact architecture and a dispensable pore-distal N-terminal blade.Cell reports · 2026Article
- Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions.Cells · 2026Review
- Soft tissue mechanosensing and remodeling: the core regulatory role of Piezo/TRPV4 ion channels.Frontiers in cell and developmental biology · 2026Review
- Brain Capillary Ion Channels: Physiology and Channelopathies.Physiology (Bethesda, Md.) · 2026Review
- Piezo1 in immune cells: from mechanosensation to immunoregulation.Frontiers in immunology · 2026Review
- PIEZO1 in Immune Cells: From Force to Function.Results and problems in cell differentiation · 2026Review
- PIPProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanotransduction mechanisms in human erythrocytes: Fundamental physiology and clinical significance.Channels (Austin, Tex.) · 2025Review
- PIEZO Force Sensing in Vascular Biology: An Explosion of New Knowledge, Concepts and Opportunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Insulin facilitates entry of calcium ions into human and murine erythrocytes via Piezo1: a newly identified mechanism with implications for type 2 diabetes.The FEBS journal · 2025Article
- Optogenetic and Endogenous Modulation of CaInternational journal of molecular sciences · 2025Review
- PIEZO1 mechanical insensitivity in generalized lymphatic dysplasia with the potential for pharmacological rescue.iScience · 2025Article
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
PIEZO channels transmit mechanical force signals to cells, allowing them to make critical decisions during development and in pathophysiological conditions. Their fast/slow inactivation modes have been implicated in mechanopathologies but remain poorly understood. Here, we report several near-atomic resolution cryo-EM structures of fast-inactivating wild-type human PIEZO1 (hPIEZO1) and its slow-inactivating channelopathy mutants with or without its auxiliary subunit MDFIC. Our results suggest that hPIEZO1 has a more flattened and extended architecture than curved mouse PIEZO1 (mPIEZO1). The multi-lipidated MDFIC subunits insert laterally into the hPIEZO1 pore module like mPIEZO1, resulting in a more curved and extended state. Interestingly, the high-resolution structures suggest that the pore lipids, which directly seal the central hydrophobic pore, may be involved in the rapid inactivation of hPIEZO1. While the severe hereditary erythrocytosis mutant R2456H significantly slows down the inactivation of hPIEZO1, the hPIEZO1-R2456H-MDFIC complex shows a more curved and contracted structure with an inner helix twist due to the broken link between the pore lipid and R2456H. These results suggest that the pore lipids may be involved in the mechanopathological rapid inactivation mechanism of PIEZO channels.
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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.