PKCζ–NADPH Oxidase–PKCα Dependent Kv1.5 Phosphorylation by Endothelin-1 Modulates Nav1.5–NCX1–Cav1.2 Axis in Stimulating Ca2+ Level in Caveolae of Pulmonary Artery Smooth Muscle Cells

Sarkar, Jaganmay; Chakraborti, Tapati; Pramanik, Pijush Kanti; Ghosh, Priyanka; Mandal, Amritlal; Chakraborti, Sajal

doi:10.1007/s12013-020-00954-x

Cited by 4 publications

(2 citation statements)

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“…R. Soc. B 378: 20220164 membrane and caveolae, where they were shown to mediate the effects of the vasoconstrictor endothelin-1 on pulmonary vascular tone [170]. Taken together, these studies suggest a potential modulatory role of Nav1.5 in SMCs with putative functional impact on various ( patho)physiological processes, but the evidence is as yet limited and further exploration is warranted.…”

Section: (C) Potential Implications For Arrhythmogenesismentioning

confidence: 88%

“…Exposure to the Nav1.5 activator veratridine or hypoxia caused vasocontraction, which was prevented by the potent Nav1.5 channel blocker F-15845; SMCs rather than endothelial cells were shown to be involved in these effects [169]. In bovine pulmonary artery SMCs, Nav1.5 expression was observed in the cell membrane and caveolae, where they were shown to mediate the effects of the vasoconstrictor endothelin-1 on pulmonary vascular tone [170]. Taken together, these studies suggest a potential modulatory role of Nav1.5 in SMCs with putative functional impact on various (patho)physiological processes, but the evidence is as yet limited and further exploration is warranted.…”

Section: Other Non-cardiomyocyte Effects Of Scn5a/nav15mentioning

confidence: 99%

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SCN5A channelopathy: arrhythmia, cardiomyopathy, epilepsy and beyond

Remme

2023

Phil. Trans. R. Soc. B

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Influx of sodium ions through voltage-gated sodium channels in cardiomyocytes is essential for proper electrical conduction within the heart. Both acquired conditions associated with sodium channel dysfunction (myocardial ischaemia, heart failure) as well as inherited disorders secondary to mutations in the gene SCN5A encoding for the cardiac sodium channel Nav1.5 are associated with life-threatening arrhythmias. Research in the last decade has uncovered the complex nature of Nav1.5 distribution, function, in particular within distinct subcellular subdomains of cardiomyocytes. Nav1.5-based channels furthermore display previously unrecognized non-electrogenic actions and may impact on cardiac structural integrity, leading to cardiomyopathy. Moreover, SCN5A and Nav1.5 are expressed in cell types other than cardiomyocytes as well as various extracardiac tissues, where their functional role in, e.g. epilepsy, gastrointestinal motility, cancer and the innate immune response is increasingly investigated and recognized. This review provides an overview of these novel insights and how they deepen our mechanistic knowledge on SCN5A channelopathies and Nav1.5 (dys)function. This article is part of the theme issue ‘The heartbeat: its molecular basis and physiological mechanisms’.

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Section: (C) Potential Implications For Arrhythmogenesismentioning

confidence: 88%

Section: Other Non-cardiomyocyte Effects Of Scn5a/nav15mentioning

confidence: 99%