Tnni3k, short for troponin I-interacting kinase, is a kinase mainly expressed in the heart [1,2,3]. It has been implicated in multiple cardiac phenotypes and physiological processes. Although its exact associated pathways remain to be fully elucidated, it appears to play a significant role in cardiac-related biological functions, making it an important target for understanding heart-related diseases [1,2]. Genetic models, such as mouse models, have been crucial in studying Tnni3k's functions [4,5].

In mice, Tnni3k has been shown to influence cardiomyocyte S-phase activity and proliferation. Retrospective analysis of single-cell ventricular suspensions in mice determined that Tnni3k definitively impacts both early and final stages of the cell cycle [4]. Additionally, studies on Tnni3k alleles in mice showed that its function is dependent on its kinase activity. Two kinase-domain frameshift mutations in mice led to loss-of-function consequences via nonsense-mediated decay. These findings suggest that Tnni3k may influence heart regenerative capacity in mice and potentially in humans as well [5].

In conclusion, Tnni3k plays essential roles in cardiomyocyte cell-cycle regulation and heart regenerative processes as revealed through mouse-based research. Mouse models, especially those with gene knockout or conditional knockout of Tnni3k, have provided valuable insights into its role in cardiac-related disease conditions such as cardiomyopathy, arrhythmias, and potentially heart failure [1,2,4,5].