Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias

Camille E Blandin (1, 2) , Basile J Gravez (3, 2) , Stéphane N Hatem (2) , Elise Balse (2)

1 BIOSCAR (UMR_S_1132 / U1132) - Biologie de l'Os et du Cartilage : Régulations et Ciblages Thérapeutiques
2 ICAN - Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases
3 CRC (UMR_S_1138 / U1138) - Centre de Recherche des Cordeliers

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.

Mots clés: trafficking; ion channels; ion channel partners; arrhythmias

Domaines: Cardiologie et système cardiovasculaire

Camille E Blandin, Basile J Gravez, Stéphane N Hatem, Elise Balse. Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias. Cells, 2021, 10 (9), pp.2417. ⟨10.3390/cells10092417⟩. ⟨hal-03367808⟩