Heart may heal with help from oxygen-sensitive genes, new study suggests

a heart attack," he continued. "But our study is the first to suggest the mechanism behind this differentiation - that a sudden exposure to higher oxygen pressure causes significant changes in the gene expression, looks and function of cardiac fibroblasts."

A heart attack occurs when a clots form, blocking blood flow through a coronary artery. Since a clot develops over time, heart cells slowly adjust to chronic hypoxia a condition of severely reduced oxygen levels. Heart cells have a tremendous ability to survive under low-oxygen conditions, said Sen, adding that sudden re-oxygenation of the tissue at the site of the clot can result in cell injury or death.

"The injured tissue is like a bull's-eye," Sen said. "This area is the most shocked by a rush of oxygen-rich blood.

"Imagine a series of concentric circles surrounding the damage oxygen shock progressively lessens the further you move away from the bull's-eye," he continued. "While the tissue in the bull's-eye is the most shocked and the heart cells here die, the shock at the perimeter of the damage is not lethal.

"This shock at the perimeter serves as a wake-up call to trigger healing. And now you have a healing band of tissue around the injured site."

It's this band of newly formed myofibroblasts that can help the heart replace tissue killed by the heart attack.

"It is important to appreciate that the heart has a built-in, healing component," Sen said. "Focusing on this healing band of tissue at the perimeter of the damaged site is likely to provide effective therapeutic solutions."

He conducted the study with Jay Zweier, Director of the Dorothy M. Davis Heart and Lung Research Institute at Ohio State; Sashwati Roy, Savita Khanna, William Wallace, Jani Lappalainen, Cameron Rink, and Arturo Cardounel, all with the Davis Heart and Lung Research Institute.


Contact: Chandan Sen
Ohio State University

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