Key result
Inhibition of the transcriptional repressor NRSF in the heart leads to cardiac dysfunction and sudden arrhythmic death accompanied by re-expression of fetal genes, including HCN and T-type Ca2+ channels.
NRSF/REST is a crucial transcriptional repressor in the heart, and its inhibition leads to pathological fetal gene re-expression, cardiac dysfunction, and sudden arrhythmic death.
Alterations in the cardiac gene program affect both cardiac structure and function, and play a key role in the progression of pathological cardiac remodeling and heart failure. For instance, reactivation of fetal cardiac genes in adults is a consistent feature of cardiac hypertrophy and heart failure. Investigation of the transcriptional regulation of cardiac genes revealed a transcriptional repressor, neuron-restrictive silencer factor (NRSF), also called repressor element-1 silencing factor (REST), to be an important regulator of multiple fetal cardiac genes. Inhibition of NRSF in the heart leads to cardiac dysfunction and sudden arrhythmic death accompanied by re-expression of various fetal genes, including those encoding fetal ion channels, such as the HCN channels and T-type Ca(2+) channels. These findings shed light on the crucial regulatory function of NRSF in the heart and its importance for maintaining normal cardiac integrity.
No takes yet. Share an insight, caveat, or question.
Koichiro Kuwahara (2013) conducted a review in Cardiac hypertrophy and heart failure. NRSF/REST inhibition was evaluated. Inhibition of the transcriptional repressor NRSF in the heart leads to cardiac dysfunction and sudden arrhythmic death accompanied by re-expression of fetal genes, including HCN and T-type Ca2+ channels.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: