Cardiac reprogramming could be the first step towards organ banking

Cardiac reprogramming could be the first step towards organ banking

Researchers at the University of Michigan may have found a way to improve heart transplant outcomes by extending the shelf life of an organ outside the body.

Dr. Paul Tang and his team found they could increase the production of a beneficial enzyme through drugs, which could potentially double the amount of time a donor heart could be in cold storage. The drug may also reduce the chances of heart transplant failure, according to the study published last week in the journal Science Transitional Medicine.

“This technology that causes donor hearts to develop adaptive responses to existence outside the body could lead to a paradigm shift in not only extending the time a heart can be outside the donor for transport, but also to improve cardiac function after transplantation,” said Dr. Tang, lead study author and heart transplant surgeon for the University of Michigan Health.

“Being able to expand core storage by uncovering the pathways that define and modulate preservation biology is the first step toward the ultimate goal of organ banking.”

Hundreds of thousands of Americans with heart failure could benefit from a transplant each year, but only about 4,000 heart transplants are performed each year, according to the University of Michigan.

The way professionals preserve organs hasn’t changed much in the past 40 to 50 years, Tang said. The idea is to keep them cold and transplant them to the recipients within four hours. Even then, transplants can fail about 10-20% of the time because stress on the heart can prevent it from pumping blood through the body properly.

The drug Tang’s team used in their study is called valproic acid. It is already approved to treat seizures, bipolar disorder and for the prevention of migraines.

In short, the drug flips a switch to produce a beneficial metabolite with antioxidant and anti-inflammatory properties. This metabolite, which is known to reduce inflammation in the presence of bacterial infection, may also reduce stress on the heart during storage/transportation.

“If you turn on this gene, it will benefit the heart by really reducing all the oxidative stress,” he said. “When you have a heart that is stored there are harmful metabolites that cause inflammation and oxidative stress and there are more of them the longer the heart is stored. By regulating this gene, we can really stop and significantly reduce the buildup effects of these harmful metabolites and also activate anti-inflammatory and antioxidant proteins.

Thanks to the drug, the heart could be stored longer, which would widen the radius at which donors and recipients could be matched.

Tang said the process could also be relevant for kidney, liver, lung and other organ transplants, as well as non-transplant surgeries where surgeons step in and stop the heart to fix a valve or do a bypass. .

Tang’s team tested the process in animal trials and in stored human hearts. The next step is to apply to the US Food and Drug Administration for permission to begin a trial involving transplant patients.

“The molecular biology field of organ preservation really doesn’t exist right now,” Tang said. “We’re starting, but that’s what we need to move forward and make the world a better place, I guess.

“It may sound like science fiction, but maybe one day, maybe 100 years from now, this could be the basis for people’s cryopreservation to go to other planets or stars. Who knows, but it have to start somewhere.

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