Table 2.

I_Na changes in TG mice with HF

Model	Cell Type	INa, A/F	SSI	SSA	INaL	INa Kinetics	SCN5A mRNA	Nav1.5 Protein	Comments (References)
CaMKIIδc-OE	V	↔	←	↔	↑	Slower recovery from inactivation and enhanced development of inactivation		↑	Trend to ↓ INa density; TG mice exhibit longer QRS intervals and monomorphic and polymorphic VT upon programmed electrical stimulation (126)
Muscle LIM protein MLP−/−	V	↓	←	→		Slowed inactivation		↓	↑ APD and EAD propensity, ↓ AP amplitude and rate of depolarization, lower Nav1.5 protein molecular weight (deglycosylation) (117)
Unilateral nephrectomy/DOCA implantation, salt water substitution	V	↓					↔	↔	Reducing mitochondrial ROS by application of NAD+, mitoTEMPO, PKC inhibitors, or PKA activators, restored INa (58)
Inducible CX43-KO	LV, RV	↓						↓	Slower conduction and longer QRS in pacing induced VT+ mice (49)
PKP2 ± ARVC	V	↓	←	↔		Slower recovery from inactivation		↔ ICC	Abnormal ultrastructure; exaggerated INa decrease and slowed conduction w/flecainide, arrhythmia and SCD (19)
ACE 8/8-OE		↔	↔ ←	←					Cardia-specific (α-MHC) overexpression; results in fourfold increase in ANG II (48, 52)
Calcineurin-OE	V	↓↓	↔	↔		↔		↔ ICC	Hypertrophy, ↓ rate of AP rise, progressive heart block, SCD (39)
Snail ± OE/DCM	V	↓					↓		DCM, ECG abnormalities, conduction defects; Homozygous mice lethal (44)
CSQ-OE	V	↓↓	→	→					DCM, hypertrophy, ↑ cell capacitance, ↑ PR and QT interval, conduction block (55)
Mdx (5cv)	V	↓					↔	↓	Dystrophin deficient; impaired conduction (35)
AnkB−/− KO	V	↓	←	←	↑	Slowed recovery from inactivation			Prolonged APD; impaired QT-rate adaptation; slowed HR; longer single Na channel mean open time; late single channel openings (23)

ACE, angiotensin-converting enzyme; ANG II, angiotensin II; ARVC, arrhythmogenic RV cardiomyopathy; CSQ, calsequestrin; DCM, dilated cardiomyopathy; KO, knockout; MHC, myosin heavy chain; MLP, muscle LIM protein; OE, overexpression; PKP2, plakophilin-2; TG, transgenic; VT, ventricular tachycardia.