Key result
NRSF/REST regulates fetal cardiac genes ANP and BNP to maintain homeostasis during pathological remodeling.
Why the study?
Reactivation of fetal cardiac genes is a key feature of pathological cardiac remodeling and heart failure, with NRSF/REST playing a pivotal role in transcriptional regulation of ANP, BNP, and other fetal cardiac genes.
This review highlights the critical role of the NRSF/REST repressor complex in regulating fetal cardiac gene expression and maintaining cardiac homeostasis during pathological remodeling.
Should not yet change heart failure management; leaves open NRSF/REST as a therapeutic research target in remodeling.
Reactivation of fetal cardiac genes, including those encoding atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), is a key feature of pathological cardiac remodeling and heart failure. Intensive studies on the regulation of ANP and BNP have revealed the involvement of numerous transcriptional factors in the regulation of the fetal cardiac gene program. Among these, we identified that a transcriptional repressor, neuron-restrictive silencer factor (NRSF), also named repressor element-1-silencing transcription factor (REST), which was initially detected as a transcriptional repressor of neuron-specific genes in non-neuronal cells, plays a pivotal role in the transcriptional regulation of ANP, BNP and other fetal cardiac genes. Here we review the transcriptional regulation of ANP and BNP gene expression and the role of the NRSF repressor complex in the regulation of cardiac gene expression and the maintenance of cardiac homeostasis.
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Inazumi et al. (2022) conducted a review in Pathological cardiac remodeling and heart failure. NRSF/REST was evaluated. The transcriptional repressor NRSF/REST plays a pivotal role in regulating fetal cardiac genes, including ANP and BNP, and maintaining cardiac homeostasis during pathological remodeling.
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