Abstract
Our group has demonstrated that 2-deoxy-ATP (dATP) improves contractility by activating myosin without affecting the relaxation at various biophysical scales, suggesting a promising sarcomere targeted candidate to mitigate cardiac dysfunction. Over-expression of ribonucleotide reductase (RNR) produces dATP in cardiomyocytes sufficient to increase contractile function. We have shown that dATP spreads between cells via gap junctions and hints that the transplantation of dATP-producing human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could significantly increase the effectiveness of cardiac cell therapy.
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