Table 1.

Atrial fibrillation (AF) susceptibility genes and loci

AF susceptibility genes			AF susceptibility loci
Gene	Mechanism	Ref.	Chromosomal locus	Candidate gene	Ref.
Potassium channel			Large-scale candidate gene or genome-wide association study
KCNQ1	Enhanced repolarization (increased IKs)	[61-65]	1q21	IL6R	[66]
KCNE1	Enhanced repolarization (increased IKs)	[9,67-69]	1q21	KCNN3	[15,16]
KCNE2	Enhanced repolarization (increased IKs)	[70]	1q24	PRRX1	[16]
KCNE5	Enhanced repolarization (increased IKs)	[71]	4q25	PITX2	[12-16]
KCNH2	Enhanced repolarization (increased IKr)	[72,73]	7q31	CAV1	[16]
KCNJ2	Enhanced repolarization (increased IK1)	[74]	9q22	C9orf3	[16]
KCNA5	Delayed repolarization and afterdepolarizations (decreased IKur)	[75]	10q22	SYNPO2L/MYOZ1	[16]
Sodium channel			14q23	SYNE2	[16]
SCN5A	Hyperpolarizing shift in inactivation (loss-of-function)/depolarizing shift in inactivation (gain-of-function)	[76-81]	15q24	HCN4	[16]
SCN1B	Decreased INa current and altered channel gating	[82]	16q22	ZFHX3	[16]
SCN2B	Decreased INa current and altered channel gating	[82]	Familial loci without known gene
Ion channel-related			6q14-q16	-	[83]
GJA5	Impaired cellular transport and intercellular electrical coupling, increased dispersion of refractoriness	[84-87]	10p11-q21	-	[88]
ANK2	Loss-of-function reduces expression and membrane targeting of Cav1.3 (decreased ICa,L)	[89,90]	10q22-q24	-	[91]
Non-ion channel
LMNA	Disruption of nuclear function or altered interaction with cytoplasmic proteins	[92-95]
NUP155	Reduced nuclear membrane permeability, enhanced repolarization	[96,97]
AGT	Unknown	[98,99]
ACE	Insertion/deletion, unknown mechanism	[100-102]
NPPA	Mutant peptide, enhanced repolarization	[103]

AF susceptibility genes were based on prior linkage mapping or candidate gene sequencing efforts. AF susceptibility loci were based on candidate gene chip or genome-wide association studies.