Key result
While viral overexpression of Tbx18 shows promise for developing a biological pacemaker, recent evidence suggests a risk of cardiac pathologies resulting from ectopic Tbx18 expression.
SAN cell clusters may drive SND; leaves open targeted molecular therapies before clinical translation.
A group of approximately 10,000 cells in the sinoatrial node (SAN), which is located at the entry of the right superior caval vein into the right atrium, is responsible for regular heart beating under different physiological conditions [1]. While the SAN is reliably working for most of our life, in the elderly, sick sinus syndrome (SSS), or sinus node dysfunction (SND) is prevalent [2] and responsible for 30 to 50% of all electronic pacemaker implantations [3]. Moreover, SSS is also often associated with the development of atrial fibrillation [4].
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Thomas Brand (2016) conducted an editorial in Sick sinus syndrome. Tbx18 gene transfer was evaluated. While viral overexpression of Tbx18 shows promise for developing a biological pacemaker, recent evidence suggests a risk of cardiac pathologies resulting from ectopic Tbx18 expression.
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