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. 2020 Dec 1;116(14):e205-e209.
doi: 10.1093/cvr/cvz283.

Cardiac arrhythmogenesis: a tale of two clocks?

Ming Lei  1 , Christopher L-H Huang  2   3
Affiliations

Cardiac arrhythmogenesis: a tale of two clocks?

Ming Lei et al. Cardiovasc Res. .
No abstract available

Keywords: Anti-arrhythmic drugs; Ca2+ homeostasis; Cardiac arrhythmias; Ion channels.

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Figures

Figure 1
Figure 1
Molecular ion channel and transporter, and signalling components contributing to normal cardiac activity and arrhythmic events and their grouping (AADs 0-VII) into pharmacological targets in the updated Oxford classification scheme. This scheme maps onto a two-clock scheme for normal and abnormal cardiac electrophysiological function. A membrane (M) clock mediates surface electrophysiological changes and conduction of excitation but feeds forwards onto the calcium (C-) clock through producing alterations in cytosolic Ca2+. These trigger cycles of store Ca2+ release and re-uptake normally driven by activation and recovery processes in the M-clock. However, the C-clock also feeds back onto the M-clock, altering AP conduction, recovery, and post-recovery stability, besides exerting longer-term effects on channel expression. Autonomic sympathetic and parasympathetic control mechanisms act at different control points respectively situated in the C- and M-clocks. cAMP, cyclic 3′5-adenosine monophosphate; Cx, connexin; Gi, inhibitory G protein; Gs, stimulatory G-protein; HCN, hyperpolarization-activated cyclic nucleotide-gated channel; MSC, mechanically sensitive channel; PKA, protein kinase A; PLB, phospholamban; RyR2, cardiac ryanodine receptor, type 2; SERCA, sarcoplasmic reticulum Ca2+-ATPase; Na+, K+ and Ca2+ flux through Nav1.5, Kv and Ca1.2 channels also shown.
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