Reperfusion therapy following an acute myocardial infarction can detrimentally increase oxidative stress and cause myocyte death. This study showed that these side effects are mediated by troponin I-interacting kinase (TNNI3K); a myocyte-specific kinase. The authors developed two TNNI3K inhibitors that reduced mitochondria-derived superoxide generation and infarct size when given during reperfusion therapy in a mouse model. Moreover, the inhibitors preserved cardiac function and limited chronic adverse remodelling, which suggests that TNNI3K is a plausible target for heart disease therapy.
References
Vagnozzi, R. J. et al. Inhibition of the cardiomyocyte-specific kinase TNNI3K limits oxidative stress, injury, and adverse remodeling in the ischemic heart. Sci. Transl. Med. 5, 207ra141 (2013)
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Harrison, C. Tinkering with heart disease. Nat Rev Drug Discov 12, 906 (2013). https://doi.org/10.1038/nrd4186
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DOI: https://doi.org/10.1038/nrd4186