When all other treatments fail, heart failure patients may be treated with a heart transplant, but finding a genetically matched donor can take more time than the patient has remaining. For decades, medical researchers have been asking whether we can find an alternative to repair a broken heart. It turns out the remedy may lie in patients’ own cells: through the process of transdifferentiation, we can transform one type of cell into another. The new cells can then be transplanted into the damaged heart. A recent experiment discovered that a cocktail of nine chemicals, “9C,” can transform cells efficiently . Scientists grew human skin fibroblasts—an abundant cell type that maintain the layered structure of skin—in a petri dish with 9C and other molecules that encourage cardiac cell growth. After a period of time, the fibroblasts turned into heart muscle cells: they gathered into well-organized stripes, they contracted together the way a complete heart beats, and they successfully repaired a damaged heart when transplanted into a mouse. These morphological and functional changes may be caused by the ability of 9C to alter genomic structures and gene expression. DNA is normally wound tightly around protein molecules, keeping it compact; 9C can loosen these structural proteins, allowing the activation of genes essential for heart function. Compared to prior genetic engineering methods, this chemical method drastically improves the efficiency of transdifferentiation. While the standard genetic engineering method only converted 0.1% of fibroblasts into cardiac cells, 9C could convert more than 97% of the cells . Although this method is still in its infancy, these results suggest it may be a promising approach to healing heart failure.
PhD Candidate, Molecular Biology Interdepartmental Doctoral Program, UCLA
 Cao, N. et al. Conversion of human fibroblasts into functional cardiomyocytes by small molecules. Science, 352, 1216–1220 (2016).
 Srivastava, D. et al. Recent advances in direct cardiac reprogramming. Current Opinion in Genetics & Development 34, 77–81 (2015).