Changing what heart cells eat could help them regenerate Consume glucose instead of fatty acids could help treat heart failure DALLAS – Feb. 20, 2020 – Switching what the powerhouses of heart cells consume for energy could help the heart regenerate when cells die, a new study led by UT Southwestern researchers suggests. Study published in Nature Metabolism, The finding, published in the Feb. 20, 2020, Nature Metabolism, could open whole new avenues for treating a variety of conditions in which heart muscle becomes damaged, including heart failure caused by viruses, toxins, high blood pressure, or heart attacks. Current pharmaceutical treatments for heart failure – including ACE inhibitors and beta blockers – center on trying to stop a vicious cycle of heart muscle loss as strain further damages remaining heart muscle, causing more cells to die, explains UT Southwestern physician-researcher Hesham A. Sadek, M.D., Ph.D., the J. Fred Schoellkopf, Jr. Chair in Cardiology. There are no existing treatments for rebuilding heart muscle. Nine years ago, Sadek and his colleagues discovered that mammalian hearts can regenerate if they’re damaged in the first few days of life, spurred by the division of cardiomyocytes, the cells responsible for a heart’s contractile force. However, this capacity is completely lost by 7 days old, an abrupt turning point in which division of these cells dramatically slows. Subsequent research has shown that this change in regenerative capacity appears to stem, at least in part, from damaging free radicals generated by organelles known as mitochondria, which power cells. These free radicals damage cells’ DNA, a phenomenon called DNA damage, which prompts them to stop dividing. The shift in free radical production appears to be spurred by a change in what mitochondria in the cardiomyocytes consume for energy, Sadek explains. Although mitochondria rely on glucose in utero and at birth, they switch to fatty acids in the days after birth to utilize these energy-dense molecules in breast milk. Sadek and his colleagues wondered whether forcing mitochondria to continue to consume glucose might stymie DNA damage and, in turn, extend the window for heart cell regeneration. To test this…