Recently, regenerative medicine using the transplantation of embryonic stem 
cells and bone marrow stem cells has been a great success but still has many 
unconfirmed problems including its clinical evaluation. The aim of this article 
is to review current literature and some patents regarding molecular therapeutic 
agents including using MAP kinase TNNI3K for the treatment and diagnosis of 
acute myocardial ischemia or infarction. TNNI3K is a novel cardiac troponin 
I-interacting kinase gene and its overexpression may promote cardiac myogenesis, 
improve cardiac performance, and attenuate ischemia-induced ventricular 
remodeling. The modulation of embryonal stem cells with high TNNI3K activity 
using a TNNI3K active peptide could be a useful therapeutic approach for 
ischemic cardiac diseases. For overexpressing TNNI3K or enhancing TNNI3K 
activity in cardiac precursor cells, the engraftment of bone marrow cells or 
embryonic stem cells can effectively promote cardiac myogenesis, beating 
frequency, and contractile functions, and decrease "silent" (no contraction) 
cardiac cells after cell transplantion, indicating that the overexpression of 
TNNI3K can increase the success rate of transplanting embryonic stem cells or 
bone marrow cells into ischemic hearts for the treatment of ischemic cardiac 
diseases. Although previous investigations showing that TNNI3K may be involved 
in the development of cardiac hypertrophy, it is still unclear whether TNNI3K 
has a role in cardiac hypertrophy or what mechanism is involved in the effects 
of TNNI3K. To confirm this, further investigations need to be undertaken.