US EditionCardiac Repair Promoted by Cyclin A2, Potential Heart Transplant Alternative
Reactivating Cyclin A2 gene prompts adult heart cells from donors aged 41 and 55 to divide and function normally, potentially enabling heart repair without transplants, study shows.
- On November 3, 2025, Mount Sinai researchers led by Hina Chaudhry reported that reactivating the Cyclin A2 gene can produce new, functioning adult human heart cells, published in npj Regenerative Medicine.
- Because adult human heart muscle cells stop dividing after birth, the heart cannot replace cells lost to heart attack or heart failure, researchers say.
- Using a replication‑deficient human‑compatible viral vector, researchers delivered CCNA2 to donor hearts aged 21, 41 and 55 and used time‑lapse imaging to confirm division in 41‑ and 55‑year‑old cells with functional daughter cells.
- The researchers plan to seek Food and Drug Administration approval to test CCNA2 therapy in patients with heart disease, aiming to let the heart heal itself and reduce transplant needs.
- Researchers caution that delivering the gene safely inside a living heart and ensuring controlled regeneration will be challenging, while Dr. Hina Chaudhry called it `This is the culmination of nearly two decades of work.
13 Articles
13 Articles
Cyclin A2 induces cytokinesis in human adult cardiomyocytes and drives reprogramming in mice - npj Regenerative Medicine
Cyclin A2 (CCNA2), a master cell cycle regulator silenced in postnatal cardiomyocytes, promotes cardiac repair in animal models. However, its effect on cytokinesis in adult human cardiomyocytes was previously unknown. We engineered a replication-deficient adenoviral vector encoding human CCNA2 under the cardiac Troponin T promoter and delivered it to freshly isolated cardiomyocytes from adult human hearts. Time-lapse live imaging revealed the in…
It "turns back time" for cells.
Specific human gene can help the heart repair itself from heart attack or heart failure
A naturally occurring gene called Cyclin A2 (CCNA2), which turns off after birth in humans, can actually make new, functioning heart cells and help the heart repair itself from injury, including a heart attack or heart failure, when the gene is turned back on.
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