Background

Cyclin A2 is the key genetic switch that mediates cardiac muscle regeneration and repair. It is the only cyclin regulating the two major checkpoints of the cell cycle, the G2/M transition and the G1/S transition. However, in mammals, cyclin A2 is silenced in hearts at birth. Mount Sinai’s researchers have demonstrated that using a gene therapy approach, cyclin A2 can be temporarily activated to induce cytokinesis in cardiomyocytes and replace heart muscle cells lost during a heart attack. The human gene therapy vector is designed to prevent oncogenicity or other adverse off-target effects.