Table 1.

A summary of mechanisms of oxidative stress induced arrhythmia and potential therapeutic targets.

Affected ion channels	Na+ current reduction (via PKC and c-Src, also via abnormal splicing) ⇒ reduction in conduction velocity
	KATP inhibition ⇒ repolarization abnormality
	NCX activation ⇒ increasing inward current and facilitating afterdepolarization
	I to, I Kr, I Ks inhibition ⇒ abnormal repolarization
	Increase in inward Ca++ current (direct or via CaMKII activation) ⇒ facilitating afterdepolarization
	Increase in late Na+current ⇒ facilitating afterdepolarization
Effect on intracellular Ca++ handling	Impairment of SERCA ⇒ increase intracellular Ca++ levels ⇒ facilitating afterdepolarization
	Affecting RyR receptor (via CaMKII activation) ⇒ leakiness of SR ⇒  increase intracellular Ca++ levels ⇒ facilitating afterdepolarization
Effect on myocyte-myocyte coupling	Affecting assembling of Cx43 at gap junctions ⇒ reduction in conduction velocity
Effect on extracellular matrix	Activating fibrotic process (via TGF-β) ⇒ reduction in conduction velocity and impaired myocyte-myocyte coupling due to collagen deposition

CaMKII: Ca²⁺/calmodulin-dependent protein kinases II; Cx43: connexin 43; NCX: Na⁺/Ca²⁺ exchanger; RyR: ryanodine receptor; SERCA: sarco-/endoplasmic reticulum Ca⁺⁺ - ATPase; TGF-β: Transforming Growth Factor-β.