Why the study?
Pathological myocardial hypertrophy is a major cause of morbidity and mortality, but understanding of its mechanism remains weak.
What is the role of NFAT3 in regulating the occurrence and progression of cardiac hypertrophy?
What is the role of NFAT3 in regulating the occurrence and progression of cardiac hypertrophy?
This review highlights the critical role of NFAT3 in the pathogenesis of cardiac hypertrophy, suggesting it as a potential therapeutic target.
NFAT3 targeting may offer a hypertrophy therapy axis; leaves open clinical translation pending validation studies.
Cardiac hypertrophy is initially an adaptive response to physiological and pathological stimuli. Although pathological myocardial hypertrophy is the main cause of morbidity and mortality, our understanding of its mechanism is still weak. NFAT3 (nuclear factor of activated T-cell-3) is a member of the nuclear factor of the activated T cells (NFAT) family. NFAT3 plays a critical role in regulating the expression of cardiac hypertrophy genes by inducing their transcription. Recently, accumulating evidence has indicated that NFAT3 is a potent regulator of the progression of cardiac hypertrophy. This review, for the first time, summarizes the current studies on NFAT3 in cardiac hypertrophy, including the pathophysiological processes and the underlying pathological mechanism, focusing on the nuclear translocation and transcriptional function of NFAT3. This review will provide deep insight into the pathogenesis of cardiac hypertrophy and a theoretical basis for identifying new therapeutic targets in the NFAT3 network.
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Wang et al. (2023) studied this question.
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