Ion Flux Dependent and Independent Functions of Ion Channels in the Vertebrate Heart: Lessons Learned from Zebrafish

Table 1

Affected ion channel and effect on heart development.

Affected ion channel	Zebrafish phenotype and effect on heart development	Reference
Na𝑣 1.5 (scn5Laa, scn5Lab)	(i) Morpholino knockdown: hypoplastic, dysmorphic heart, reduced numbers of cardiomyocytes; (ii) pharmacological modification: normal heart tube formation	[17]
LTCC α1C subunit	(i) Island beat (isl): loss of function; hypoplastic and silent ventricle, reduced numbers of ventricular cardiomyocytes; atrial fibrillation	[28]
LTCC β2.1 subunit	(i) Morpholino knockdown: defects in cardiac looping and ballooning, reduced numbers and proliferation of cardiomyocytes, disrupted cell integrity; bradycardiac and weakly contractile heart rhythm; (ii) pharmacological modification with nifedipin resembles the morphants’ phenotype	[29]
NCX1h	(i) Tremblor (tre): loss of function; hypoplastic and nearly silent ventricle, disruptions of sarcomere assembly in the ventricle; atrial fibrillation	[35]
SERCA2a	(i) Morpholino knockdown, pharmacological modification: absent cardiac looping, no expanding of cardiac chambers, bradycardia	[35]
Na^+K^+-ATPase α1B1 subunit	(i) heart and mind (had): loss of function, disturbed heart tube elongation and cardiogenic differentiation	[45]
Na^+K^+-ATPase α2 subunit	(i) Morpholino knockdown: perturbed cardiac looping and laterality	[45]
zERG	(i) reggae (reg): gain of function; Short-QT-Syndrome, no effect on heart development; (ii) breakdance (bre): loss of function; Long-QT-Syndrome, no effect on heart development; (iii) S290^−/−, S213^−/−: loss of function; Long-QT-Syndrome; (iv) Morpholino knockdown, pharmacological modification: no effects on heart development	[46–51]