Heart repair: A gene that normally shuts down after birth may hold the key to repairing damaged hearts. Researchers at Mount Sinai report that reactivating Cyclin A2 (CCNA2) can push adult human heart muscle cells to divide and form new, functioning tissue, offering a potential alternative to transplants or implanted devices. The findings appear in npj Regenerative Medicine.
Led by Dr Hina Chaudhry, Director of Cardiovascular Regenerative Medicine at the Icahn School of Medicine at Mount Sinai, the team used a human-compatible, replication-deficient viral vector to deliver CCNA2 into adult human cardiomyocytes cultured from healthy donor hearts. Time-lapse imaging showed the treated cells re-entered the cell cycle and split into daughter cells that retained normal structural proteins and calcium handling, indicating they remained functional rather than reverting to an immature state.
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Cells from 41- and 55-year-old donor hearts responded robustly to CCNA2, while cells from a 21-year-old heart did not, consistent with earlier work suggesting younger hearts have more baseline regenerative capacity. The mechanism appears to “briefly turn back the clock” on growth pathways without triggering harmful thickening or loss of specialisation.
The work builds on Chaudhry’s 2014 porcine study showing CCNA2 could regenerate large-mammal hearts after myocardial infarction. The new paper provides a translational step, demonstrating that a delivery method suitable for people can safely induce division in adult human heart cells.
The heart muscle lost after a heart attack or heart failure does not naturally regrow, leaving patients with permanent deficits. By reawakening a silenced, naturally occurring pathway, CCNA2 therapy could change that calculus.
