TNNI3K is a new cardiac-specific MAP kinase whose gene is localized to 1p31.1 
and that belongs to a tyrosine kinase-like branch in the kinase tree of the 
human genome. In the present study we investigated the role of TNNI3K in the 
cardiac myogenesis process and in the repair of ischemic injury. Pluripotent 
P19CL6 cells with or without transfection by pcDNA6-TNNI3K plasmid were used to 
induce differentiation into beating cardiomyocytes. TNNI3K promoted the 
differentiation process, judging from the increasing beating mass and increased 
number of alpha-actinin-positive cells. TNNI3K improved cardiac function by 
enhancing beating frequency and increasing the contractile force and epinephrine 
response of spontaneous action potentials without an increase of the single-cell 
size. TNNI3K suppressed phosphorylation of cardiac troponin I, annexin-V(+) 
cells, Bax protein, and p38/JNK-mediated apoptosis. Intramyocardial 
administration of TNNI3K-overexpressing P19CL6 cells in mice with myocardial 
infarction improved cardiac performance and attenuated ventricular remodeling 
compared with injection of wild-type P19CL6 cells. In conclusion, our study 
clearly indicates that TNNI3K promotes cardiomyogenesis, enhances cardiac 
performance, and protects the myocardium from ischemic injury by suppressing 
p38/JNK-mediated apoptosis. Therefore, modulation of TNNI3K activity would be a 
useful therapeutic approach for ischemic cardiac disease.