The inability of heart cells to divide rapidly enough to repair damage is a major impediment to regenerating heart tissue after myocardial infarction. A U.S. team has used cyclin A2 gene therapy to induce cardiomyocyte division and improve heart function in pig models of MI.
Loss-of-function mutations in chromatin-modifying proteins remain largely intractable. Separate teams, including a group from Novartis, have identified synthetic lethal interactions that could be exploited to help treat cancers with mutations in the SWI/SNF chromatin-remodeling complex.
A U.S. team has leveraged the cardioprotective activity of TIMP3 using a formulation and delivery strategy that avoids off-target effects. Preclinical data indicate that the procedure could help prevent heart failure after myocardial infarction, but identifying the right patients could be a challenge.