ArticleFrontiers in physiology2011
Voltage-gated channel mechanosensitivity: fact or friction?
Article in Frontiers in physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 95 citations in OpenAlex.
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- A Novel Function of NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Modeling autoregulation of cardiac excitation-Ca-contraction and arrhythmogenic activities in response to mechanical load changes.iScience · 2025Article
- Piezo channels modulate human lung fibroblast function.American journal of physiology. Lung cellular and molecular physiology · 2024Article
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- Single-neuron mechanical perturbation evokes calcium plateaus that excite and modulate the network.Scientific reports · 2023Article
- Mechanosensitive aquaporins.Biophysical reviews · 2023Review
- The Voltage-Gated Sodium Channel ineNeuro · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Tetrodotoxin Decreases the Contractility of Mesenteric Arteries, Revealing the Contribution of Voltage-Gated NaMarine drugs · 2023Article
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- Capsaicin as an amphipathic modulator of NaChannels (Austin, Tex.) · 2022Article
- Ectopic foci do not co-locate with ventricular epicardial stretch during early acute regional ischemia in isolated pig hearts.Physiological reports · 2022Article
- Physics of mechanotransduction by Piezo ion channels.The Journal of general physiology · 2022Review
- Quantum Mechanical Aspects in the Pathophysiology of Neuropathic Pain.Brain sciences · 2022Article
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- The Quantum Tunneling of Ions Model Can Explain the Pathophysiology of Tinnitus.Brain sciences · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heart is a continually active pulsatile fluid pump. It generates appropriate forces by precisely timed and spaced engagement of its contractile machinery. Largely, it makes its own control signals, the most crucial of which are precisely timed and spaced fluxes of ions across the sarcolemma, achieved by the timely opening and closing of diverse voltage-gated channels (VGC). VGCs have four voltage sensors around a central ion-selective pore that opens and closes under the influence of membrane voltage. Operation of any VGC is secondarily tuned by the mechanical state (i.e., structure) of the bilayer in which it is embedded. Rates of opening and closing, in other words, vary with bilayer structure. Thus, in the intensely mechanical environment of the myocardium and its vasculature, VGCs kinetics might be routinely modulated by reversible and irreversible nano-scale changes in bilayer structure. If subtle bilayer deformations are routine in the pumping heart, VGCs could be subtly transducing bilayer mechanical signals, thereby tuning cardiac rhythmicity, collectively contributing to mechano-electric feedback. Reversible bilayer deformations would be expected with changing shear flows and tissue distension, while irreversible bilayer restructuring occurs with ischemia, inflammation, membrane remodeling, etc. I suggest that tools now available could be deployed to help probe whether/how the inherent mechanosensitivity of VGCs - an attribute substantially reflecting the dependence of voltage sensor stability on bilayer structure - contributes to cardiac rhythmicity. Chief among these tools are voltage sensor toxins (whose inhibitory efficacy varies with the mechanical state of bilayer) and arrhythmia-inducing VGC mutants with distinctive mechano-phenotypes.
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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.