Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias

Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias

Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Vol. 10; no. 9; p. 2417
Main Authors: Blandin, Camille E., Gravez, Basile J., Hatem, Stéphane N., Balse, Elise
Format: Journal Article
Language:English
Published: Basel MDPI AG 14-09-2021
MDPI
Subjects:
Arrhythmia
arrhythmias
Cardiac arrhythmia
Cardiology and cardiovascular system
Cardiomyocytes
Fibrosis
Heart failure
Human health and pathology
ion channel partners
Ion channels
Kinases
Life Sciences
Mutation
Myocytes
Plasma
Post-transcription
Potassium
Potassium channels (voltage-gated)
Proteins
Review
trafficking
arrhythmias
trafficking
ion channel partners
ion channels
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Summary:Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be a major source of channel dysfunction during cardiac arrhythmias. This has been well established with the discovery of mutations in the genes encoding several ion channels and ion channel partners during inherited cardiac arrhythmias. Fibrosis, altered myocyte contacts, and post-transcriptional protein changes are common factors that disorganize normal channel trafficking during acquired cardiac arrhythmias. Channel availability, described notably for hERG and KV1.5 channels, could be another potent arrhythmogenic mechanism. From this molecular knowledge on cardiac arrhythmias will emerge novel antiarrhythmic strategies.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Review-1
ISSN:2073-4409
2073-4409
DOI:10.3390/cells10092417