Key result
TNNI3K regulates cardiac hypertrophy, conduction, and ischemia/reperfusion injury, emerging as a potential therapeutic target.
Why the study?
Several new papers on TNNI3K have been published since the last overview, broadening the clinical perspective of TNNI3K variants and our understanding of the underlying molecular biology.
This review highlights the emerging role of the cardiac-specific kinase TNNI3K in arrhythmias and cardiomyopathies, and its potential as a novel therapeutic target.
Requires prospective trials before targeting TNNI3K clinically; extends genetic and preclinical associations but remains hypothesis-generating.
In the two decades since the discovery of TNNI3K it has been implicated in multiple cardiac phenotypes and physiological processes. TNNI3K is an understudied kinase, which is mainly expressed in the heart. Human genetic variants in TNNI3K are associated with supraventricular arrhythmias, conduction disease, and cardiomyopathy. Furthermore, studies in mice implicate the gene in cardiac hypertrophy, cardiac regeneration, and recovery after ischemia/reperfusion injury. Several new papers on TNNI3K have been published since the last overview, broadening the clinical perspective of TNNI3K variants and our understanding of the underlying molecular biology. We here provide an overview of the role of TNNI3K in cardiomyopathy and arrhythmia covering both a clinical perspective and basic science advancements. In addition, we review the potential of TNNI3K as a target for clinical treatments in different cardiac diseases.
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Pham et al. (2021) conducted a review in Cardiac Disease. TNNI3K inhibitors and genetic variants was evaluated. TNNI3K expression and genetic variants influence cardiac hypertrophy, conduction, and response to ischemia/reperfusion injury, highlighting its potential as a therapeutic target for cardiac diseases.
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