Some forms of heart disease manifest via the hyperactivation of specific proteins. One protein in particular, CaMKII delta, can cause heart failure, arrhythmia (irregular heartbeat), and post-heart attack damage to the heart’s muscle tissue when hyperactivated. CaMKII delta and other proteins are produced by the body according to DNA’s instructions, meaning the problem can be blamed (at least in part) on DNA itself.
Eric Olson, a molecular biologist at the University of Texas Southwestern Medical Center, has created an iteration of the 20-year-old CRISPR technique that facilitates acute DNA editing to eliminate CaMKII delta hyperactivation. CRISPR, a mechanism by which molecular scissors cut genetic material from any living being, has previously (and controversially) been used to edit the DNA of plants, mosquitoes, and even humans. Now Olson’s version has been proven to be effective in mice.
(Image: Robina Weermeijer/Unsplash)
In an experiment described in the journal Science last week, Olson’s team used what they call a “fine-tipped” ablation pen to change a couple of adenine compounds to guanine within mouse DNA. This effectively changed the DNA’s instructions for CaMKII delta production, preventing the protein from being hyperactivated. When Olson and his colleagues tested this in mice that had endured heart attack-related cardiac damage, the rodents’ hearts recovered. They found similar success following tests with cardiomyocytes (cells that govern heart contractions) derived from human stem cells. Better yet, once the “editing” process was complete, it took care of CaMKII delta’s hyperactivation permanently; there was no need to repeat the procedure.
Heart disease is a globally ubiquitous killer. In the US alone, more than 800,000 people have a heart attack each year. While not all of these are fatal, nearly all cause some degree of damage to the heart’s muscle tissues, which makes it harder for a survivor to withstand future heart attacks or other major health issues. A procedure like the one performed by Olson’s team could extend the lives of hundreds of thousands of people each year—if, of course, it proves effective in humans. Olson himself has said the gene editing process could differ in humans (or even other primates) due to physiological differences. If it works, however, it could someday permanently resolve people’s cardiac risks with a single procedure.
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