It was essential, Ashley said, to have the healthy donor hearts available.
To date, studies that compare the genomics of healthy hearts and heart failure have taken place mainly in mice. But with the healthy donor heart tissue, the team was able to compare and contrast genomic information in human hearts. They found that fewer biological pathways were involved in heart failure compared with healthy hearts, but there were more genes involved in those pathways.
Perhaps most telling, PPP1R3A had one of the biggest leaps in gene connectivity during the transition to heart failure, meaning it became associated with the activity of many other genes.
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PPP1R3A as a central regulator makes sense because the gene plays a critical role in the metabolism of glucose within cells, Ashley said. It turned out that mice lacking the PPP1R3A gene maintained normal heart function, whereas those with the gene succumbed to heart failure. If we were able to inhibit this gene somehow in humans, we could potentially have a therapeutic drug that could protect patients from heart failure.
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Stanford Medicine's unrivaled atmosphere of breakthrough thinking and interdisciplinary collaboration has fueled a long history of achievements. View timeline. Gene networks reveal transition from healthy to failing heart. Jun 24 Tracking the transition Heart failure is not one simple condition, said Ashley, who treats cardiac patients at Stanford Health Care.
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Gene networks reveal transition from healthy to failing heart
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