Abstract
Our group has demonstrated that 2-deoxy-ATP (dATP) improves contractility by activating myosin without affecting the relaxation, from the myofibril to the animal level, suggesting a promising candidate to mitigate cardiac dysfunction. Ribonucleotide Reductase (RNR), a rate-limiting enzyme for de novo synthesis of deoxynucleotides, produces dATP in cells. We have shown that dATP spreads between cells via gap junctions and hints us that the transplantation of dATP-producing human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could significantly increase the effectiveness of cardiac cell therapy against HF.
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