ArticlePflugers Archiv : European journal of physiology2019
β1 and β3 subunits amplify mechanosensitivity of the cardiac voltage-gated sodium channel Nav1.5.
Article in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
- A Novel Function of NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The dispensability of 14-3-3 proteins for the regulation of human cardiac sodium channel Nav1.5.PloS one · 2024Article
- Tetrodotoxin Decreases the Contractility of Mesenteric Arteries, Revealing the Contribution of Voltage-Gated NaMarine drugs · 2023Article
- Roles of stretch-activated channels and NADPH oxidase 2 in the induction of twitch contraction by muscle stretching in rat ventricular muscle.Pflugers Archiv : European journal of physiology · 2022Article
- Cell-Adhesion Properties of β-Subunits in the Regulation of Cardiomyocyte Sodium Channels.Biomolecules · 2020Review
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In cardiomyocytes, electrical activity is coupled to cellular contraction, thus exposing all proteins expressed in the sarcolemma to mechanical stress. The voltage-gated sodium channel Nav1.5 is the main contributor to the rising phase of the action potential in the heart. There is growing evidence that gating and kinetics of Nav1.5 are modulated by mechanical forces and pathogenic variants that affect mechanosensitivity have been linked to arrhythmias. Recently, the sodium channel β1 subunit has been described to stabilise gating against mechanical stress of Nav1.7 expressed in neurons. Here, we tested the effect of β1 and β3 subunits on mechanosensitivity of the cardiac Nav1.5. β1 amplifies stress-induced shifts of V
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