Table 1.

Genome-Wide Studies using the zebrafish model to validate the causality of candidate genes.

Genome-wide study	Disease	Gene(s)	Zebrafish genetic tool	Zebrafish phenotype	References
(74): GWAS in 1,910 patients/3,630 controls	DCM	HSPB7	MO knockdown TALEN knockout	Heart looping defects Increased susceptibility to cardiomyopathy	(75, 76)
(77): GWAS in 1,590 patients/577 controls	HF	HSPB7
(78): GWAS in 1,179 patients/1,108 controls	DCM	BAG3	MO knockdown	Cardiac and skeletal myopathy	(79, 80)
(79): WES in one multigeneration family	DCM	BAG3
(81): WES in three multigeneration families	DCM	FLNC	MO knockdown	Abnormal cardiac function and structure	Same study (80)
(82): WES on three unrelated probands	AF	KCNIP1	Overexpression MO knockdown	Overexpression promotes AF	Same study
(83): Combined genetic and proteomic GWAS of 4 cohorts with 17,692 samples	LQTS	VCL	MO knockdown Gene-Trap CRISPR/Cas9	Defective cardiac repolarization Myocardial contractile dysfunction	Same study (84, 85)
(86): WES on three cases	CAID	SGOL1	MO knockdown	Bradycardia	Same study
(87): GWAS in 590 patients/732 controls	DCM	HBEGF, IK, SRA1	MO knockdown	Myocardial contractile dysfunction	Same study

Mentioned here are examples found by manual database analysis. The list might not be exhaustive.

AF, atrial fibrillation; CAID, Chronic atrial and intestinal dysrhythmia; DCM, dilated cardiomyopathy; GWAS, genome-wide association study; HF, heart failure; LQTS, long QT syndrome; MO, morpholino; WES, whole exon sequencing.