Your heart beats about 35 million times in a single a year. That’s a whopping number of beats—each generated by electrical signals that make the heart contract. Occasionally problems with heart’s electrical system can cause irregular rhythms, or arrhythmias. Some types of arrhythmias are merely annoying; others can last long enough to affect how the heart works, or even cause sudden cardiac arrest.

Although certain arrhythmias can be successfully treated with medication, surgery and/or devices such as pacemakers, cardiac disorders and heart disease still account for more deaths than any other disease.

Finding new treatments for arrhythmias requires a deep understanding of how the heart beats, and specifically the intricate electrical system that prompts the heart to contract. It also requires a model to study. Is Drosophila melanogaster—a type of fruit fly—the answer?

Using flies to study the heart

Both the human heart and fly hearts have four chambers and both start out as linear tubes in embryos—but ours loops during development to form a more compact structure where as a the fly heart does not. Despite this structural difference there are many functional similarities between the fly and human heart.

“One of the similarities that we focus on in my lab is the way ion channels work—and don’t work—to fully understand how faulty ion channels contribute to heart arrhythmias,” says Karen Ocorr, PhD, assistant professor at SBP.

Ion channels are proteins found in cell membranes that allow specific ions such as potassium, sodium and calcium, to pass through cells. When ion currents travel into heart muscle cells, the muscle becomes depolarized, creating an electrical current that causes the heart to contract. A second set of channels are important in repolarization of the heart, which allows it to relax and refill with blood.

In her new paper published in PLOS Genetics, Ocorr describes how two repolarizing potassium ion channels called hERG and KCNQ control the rate and efficiency of fly heart contractions—similar to their role in human heart muscle. The research also shows that mutations in hERG and KCNQ lead to arrhythmias that worsen with age—as they do in humans.

“In humans, when hERG is compromised, either by drugs or inherited mutations, hearts can take longer than normal to recharge between beats, causing a potentially fatal condition called long QT syndrome. In fact, some anti-arrhythmia drugs actually cause long QT syndrome, hence the need for better, more specific therapies,” explains Ocorr.

The capacity for drugs to cause long QT syndrome has led the Food and Drug Administration (FDA) to recommend including the evaluation of new cardiac and non-cardiac drugs for this possible side effect. The FDA is the United States agency that provides licenses to market new drugs.

Interestingly, neither of the ion channels we identified in the fly heart play a major role in the adult mouse heart, ruling it out as useful model to screen for drug-related long QT effects,” says Ocorr.

“We are encouraged that Drosophila may become an easy, accurate tool to pre-clinically screen for adverse cardiac events associated new anti-arrhythmia therapies—potentially making the next drug discovery for patients happen sooner.”

Read the paper here.