Heart cells: no longer undivided

The inability of adult heart cells to divide rapidly enough to repair cardiac damage has been a major impediment to regenerating heart tissue and preventing fibrosis after myocardial infarction. Now, a U.S. team has used cyclin A2 gene therapy to induce cardiomyocyte division and improve heart function in pig models of myocardial infarction.1

The technology has been licensed to VentriNova Inc., which is planning IND-enabling studies and is seeking investors to fund clinical testing of cyclin A2 (CCNA2) gene therapy to treat MI.

Most mammalian cells regenerate their tissues after injury by undergoing mitosis, but cardiomyocytes do not. Instead, cardiac fibroblasts proliferate after MI. Although they replace the damaged tissue and thus maintain the organ's structural integrity,2,3 they result

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