Nature Journal Club

Paul Riley

University College London

A molecular cardiologist looks into getting to the heart of his inner fish.

Newts do it, fish do it, but sadly humans and other mammals cannot repair or regenerate damaged heart tissue as adults.

Despite the modern-day promotion of healthier lifestyles (such as bans on smoking in public places and pro-fitness campaigns in the run-up to London 2012), cardiovascular disease is still on the up worldwide and, not unlike swine flu, is a true pandemic that respects no borders. As a result, and for some time now, I and others have been asking how we might become more newt-like or fish-like and repair our own hearts after a heart attack.

We have favoured looking at small resident progenitor cells which, when stimulated, might make new heart muscle and blood vessels. But a study by Bernhard Kühn and his colleagues at the Children’s Hospital Boston in Massachusetts shows us another way (K. Bersell et al. Cell 138, 257–270; 2009).

They simply asked whether or not existing heart muscle can be instructed to divide and make more of the same. Apparently it can, with the help of the epidermal growth factor neuregulin (famed for its role in the nervous system), and its Erb4 receptor. While under the influence of neuregulin, some mature heart cells in mice disassemble their scaffold, re-enter the cell cycle, divide and regenerate injured muscle.

Of course, the devil is in the detail: the trick, it seems, is to have not only plenty of neuregulin, but also more heart muscle cells with one nucleus instead of two, because only the former responded to the growth factor. Unfortunately, this presents something of a conundrum where mammals are concerned. Mammalian heart-muscle cells generally become binuclear shortly after birth. Thus, for a complete fix, we are left heading back in the direction of the drawing board.

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