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Rescuing Injured Hearts by Enhancing Regeneration

Using a two-drug approach, researchers at Children’s Hospital Boston have demonstrated that it may be possible to rescue heart function //after a heart attack and protect the heart from scarring. Working with rats, they combined an agent that overcomes a natural inhibitor of cell division with a naturally occurring growth factor that encourages blood vessel growth (angiogenesis). Together, these two agents enabled heart-muscle cells to multiply and the heart to regain its function after a simulated myocardial infarction.

Normally, after a heart attack, the damaged heart muscle cannot grow back and is instead replaced by scar tissue. Excessive scarring can impair the heart’s pumping capacity and can lead to life-threatening arrhythmias. Heart-muscle cells (cardiomyocytes) normally cannot replicate in mammals, a major obstacle to regeneration. However, in a paper last year, Felix Engel, PhD, and Mark Keating, MD, in the Department of Cardiology at Children’s Hospital Boston, showed that they could coax cardiomyocytes to multiply in a petri dish by inhibiting an enzyme known as p38 MAP kinase, which normally suppresses cardiomyocyte replication. [See: http://www.childrenshospital.org/newsroom
/Site1339/mainpageS1339P1sublevel139.html]

Engel and Keating (Keating is now at the Novartis Institute for BioMedical Research) now build on this finding. They studied 120 rats, some with simulated heart attacks. After the injury, the animals were randomly assigned to receive injections with a p38 MAP kinase inhibitor alone, the angiogenesis stimulator FGF1 alone, both agents together, or saline (placebo) for four weeks. Three months later, rats that had received both FGF1 and the p38 MAP kinase inhibitor had markedly improved heart function, as measured on echocardiograms: their hearts pumped almost as well as the hearts of uninjured rats. They also had reduced thinning of the cardiac wall and the least amount of scarring.

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