Staying Off the Beating Track

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Science  30 Oct 2009:
Vol. 326, Issue 5953, pp. 644
DOI: 10.1126/science.326_644a

DCT expression in mouse heart.

CREDIT: LEVIN ET AL., J. CLIN. INVEST. 119, 10.1172/JCI39109 (2009)

Atrial fibrillation, the most common heart arrhythmia observed in the clinic, occurs when the heart's normal pacemaker activity is disrupted by an aberrant electrical stimulus that in many cases originates in the pulmonary veins. Although individuals with cardiovascular disease are often affected, atrial fibrillation can also arise in healthy folks, and the cellular mechanisms that launch and maintain it are not fully understood. To date, research and treatment efforts have focused on pulmonary vein myocytes as the source of the electrical activity that triggers atrial arrhythmias.

Levin et al. describe an unusual cell type whose dysfunction can initiate atrial arrhythmia—at least in mice. These cells, referred to as cardiac melanocytes because they express the melanin synthetic enzyme dopachrome tautomerase (DCT), reside in regions associated with atrial arrhythmia (for instance, in the pulmonary veins and atria) and in culture, display action potentials resembling those of atrial myocytes. Mice lacking cardiac melanocytes are more resistant than wild-type mice to treatments that induce atrial arrhythmias. Furthermore, the enzyme DCT functions as more than a cell marker; mice that lack DCT are more susceptible to atrial arrhythmias, suggesting that this enzyme reduces the likelihood of ectopic electrical activity, possibly via buffering of intracellular calcium and reactive oxygen species. Cardiac melanocytes are also present in relevant areas of the human heart and pulmonary veins, but whether they contribute to atrial fibrillation in humans remains to be determined.

J. Clin. Invest. 119, 10.1172/JCI39109 (2009).

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