May 9 (UPI) — A simple single gene-editing approach may help to prevent heart arrhythmia — an abnormal heartbeat — in mice and offers promise for humans to avoid complications after a heart attack.

An international collaboration of researchers seeking to deal with damaged hearts and the effects of that damage found in a recent study with mice that gene therapy may correct the damage. Their findings were published Tuesday in the journal Nature Scientific Reports.

About 2 percent of people younger than age 65 have arrhythmia, or AFib, and about 9 percent of people aged 65 years or older have the condition, according to the Centers for Disease Control and Prevention.

In the trial, the group delivered a single gene called Connexin43, or Cx43, through a single virus injection into the scar tissue of mice.

“It could be a very simple medical procedure,” Dr. Michael Kotlikoff, a provost at Cornell University and a professor of molecular physiology, said in a press release. “One could imagine a relatively noninvasive procedure in which the gene is introduced through a catheter, resulting in long-term protection.”

During a heart attack, or myocardial infarction, heart muscle cells are replaced by fibroblasts and new blood vessels. But they don’t conduct electricity leaving the heart susceptible to ventricular tachycardia, which is an excessive heart rate that can result in sudden death.

It’s critical for the heart to have a normal pattern of electrical conduction through these non-heart cells in order to work properly.

In a paper published in 2007, this same team transplanted living embryonic heart muscle cells into the cardiac tissue of mice that had suffered heart attacks — the mice became resistant to cardiac arrhythmias.

In the new study, the Cx43 protein cells were electrically coupled to each other and with normal heart cells, a process known as heterotypic cell-cell coupling. And with greatly enhanced conductivity, the researchers report there was long-lasting protection from arrhythmia.

“We’ve created a bridge for the electrical signal,” Dr. Bernd Fleischmann, professor and chairman of the Institute of Physiology at the University of Bonn. “We suspected it would work. We suspected that the cells we were putting in were actually working in this way, but it is really exciting.”

But the researchers aren’t sure it will be as effective in humans because mouse hearts are so much smaller and shaped differently.

“Whether this will work in humans, or even in larger animals, that’s still a question and my colleagues in Germany are pursuing this,” Kotlikoff said.

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