Table 1.

Impact of mitochondrial dysfunction on cardiac arrhythmogenicity

Target Channel/Transporter	Impact of Mitochondrial Dysfunction	Impact on electrical/ionic homeostasis	Pro-arrhythmic mechanism
Peak I_Na	↓	↓ Na⁺ influx	Slow conduction
Late I_Na	↑	↑ Na⁺ influx, prolonged APD	EAD
I_to	↓	↓ K⁺ influx, prolonged APD	EAD
I_CaL	±
I_K	↓	↓ K⁺ influx, prolonged APD	EAD
I_K1	↓	↓ K⁺ influx, prolonged APD	EAD
I_KATP	↑	↑ K⁺ influx, shortened APD	Current sink, slow conduction
NCX	↑	Cytosolic Ca²⁺ overload	DAD
Cx43	↓	Impaired gap junction function	Slow conduction
SERCA	↓	Cytosolic Ca²⁺ overload	DAD
RyR2	↑	Cytosolic Ca²⁺ overload	DAD
mitoNCX	Reverse mode	Cytosolic Ca²⁺ overload	DAD
mitoK_ATP/mitoK_Ca	↑	↑Mitochondrial K⁺ influx	Protective, mechanism of ischemic-preconditioning

Peak I_Na: peak Na⁺ current; Late I_Na: late Na⁺ current; I_to: transient outward K⁺ current; I_CaL: L-type Ca²⁺ current; I_K: delayed rectifier K⁺ current; I_K1: inwardly rectifying K⁺ current; I_KATP: ATP-sensitive K⁺ current; NCX: Na⁺/Ca²⁺ exchanger; Cx43: connexin 43; SERCA: sarco/endoplasmic reticulum Ca²⁺-ATPase; RyR2: ryanodine receptor 2; mitoNCX: mitochondrial Na⁺/Ca²⁺ exchanger; mitoK_ATP: mitochondrial ATP-sensitive K⁺ current; mitoK_Ca: mitochondrial Ca²⁺-sensitive K⁺ current; APD: action potential duration; EAD: early after-depolarization; DAD: delayed after-depolarization.