1. Cardiac troponin I-interacting kinase (TNNI3K) is a novel cardiac-specific 
kinase gene. Quantitative real-time reverse transcription polymerase chain 
reaction analysis showed a significant increase in TNNI3K mRNA expression in 
hypertrophic cardiomyocytes induced by endothelin-1 (ET-1). The aim of the 
present study was to investigate the effects of TNNI3K on neonate rat 
cardiomyocyte hypertrophy induced by ET-1. 2. Adenoviruses were amplified in 
293A cells. To determine a reasonable adenovirus infection dose cardiomyocytes 
were infected with an adenovirus carrying human TNNI3K (Ad-TNNI3K) at varying 
multiplicity of infection (MOI) and the expression of TNNI3K was analysed by 
western blot. 3. Cardiomyocytes were infected with either a control adenovirus 
carrying green fluorescent protein (Ad-GFP) or Ad-TNNI3K. Compared with Ad-GFP, 
the Ad-TNNI3K induced an increase in sarcomere organization, cell surface area, 
(3) H-leucine incorporation and β-MHC re-expression. This type of hypertrophic 
phenomenon is similar to that observed in Ad-GFP-infected hypertrophic 
cardiomyocytes induced by ET-1. To determine the functional role of TNNI3K in 
ET-1-induced hypertrophic cardiomyocytes, the cells were infected with Ad-GFP or 
Ad-TNNI3K. Ad-TNNI3K induced an increase in sarcomere organization, cell surface 
area and (3) H-leucine incorporation compared with Ad-GFP. 4. These results 
suggest that TNNI3K overexpression induces cardiomyocytes hypertrophy and 
accelerates hypertrophy in hypertrophic cardiomyocytes. Therefore, TNNI3K might 
be an interesting target for the clinical treatment of hypertrophy.