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The Cutting Edge

Heart’s Repair Process Points to New Treatment Strategy for Heart Attack

  new strategy for treating people who have suffered a heart attack  
  Image shows scar-forming cells (in red) in a region of the injured heart expressing endothelial marker (in green) and thus appearing yellow (arrows). The study observed that approximately a third of the scar-forming cells in the injured region of the heart adopted endothelial blood-vessel-cell-like characteristics.
Image: Courtesy of Dr. Arjun Deb

UCLA researchers have discovered that fibroblasts — scar-forming cells in the heart — have the ability to become endothelial cells, the cells that form blood vessels. Because increasing the number of blood vessels in the heart boosts its ability to heal after injury, the finding could point the way toward a new strategy for treating people who have suffered a heart attack.

Reversing or preventing scar tissue from forming has been one of the major challenges of cardiovascular medicine, says Arjun Deb, MD, associate professor of medicine in the Division of Cardiology and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “It is well-known that increasing the number of blood vessels in the injured heart following a heart attack improves its ability to heal. And we know that scar tissue in the heart is associated with a poorer prognosis. Our findings suggest the possibility of coaxing scar-forming cells in the heart to change their identity into blood-vessel-forming cells, which could potentially be a useful approach for better heart repair.”

Several years ago, Dr. Deb and his colleagues were investigating the relationship between fibroblasts and endothelial cells, which exist in close proximity in the injured heart. Through experiments in mice in which scar-forming cells in the heart were genetically labeled, the researchers discovered that many of the fibroblasts in the heart’s injured region changed into endothelial cells and contributed directly to blood-vessel formation — a phenomenon they called mesenchymal-endothelial transition, or MEndoT. The researchers identified a molecular mechanism that regulated MEndoT and found that administering a small molecule to augment MEndoT led to less scarring and allowed the heart to heal more completely. They plan to test similar small molecules in other models to determine whether or not the strategy could potentially be used to benefit humans.

“There are remarkable similarities in the process of scarring in different organs after injury,” Dr. Deb says. “Our hope is that this approach can be used to treat scar tissue in other organs as well.”

“Mesenchymal-endothelial transition contributes to cardiac neovascularization,” Nature, October 15, 2014

 





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