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The human heart possesses stem cells but cannot regenerate after injury, instead replacing damaged muscle with scar tissue. Our powerlessness to mend an ailing heart is the primary cause of death in the developed world.
In May cardiologist Mark T. Keating of Harvard Medical School and his colleagues accomplished the long-sought goal of enticing adult mammal heart muscle cells to multiply, the first step on the road to heart-repair therapies. In 2002 Keating discovered that zebra fish could regrow up to a fifth of their hearts within two months without scarring following removal of 20 percent of the muscle from the lower chamber. He then sought to achieve the same results in humans. His laboratory found that activity of the enzyme p38 MAP kinase was lowest in fetal rats when the heart was growing and highest when heart muscle cell growth slowed or halted, suggesting it put the brakes on cell division.
When the researchers partnered a p38-inhibiting drug with growth factor FGF1, this combination spurred adult rat heart muscle cells to proliferate. Keating and his team believe a drug-based approach to repairing hearts could prove more elegant than ones based on stem cells. The scientists are currently testing mixtures of p38 inhibitor and growth factor on animals that have suffered heart attacks to see if they can help the body's most important muscle heal. Such drugs would mark a revolution in cardiology.
