Uncovering a link between inflammation and heart disease

Looking at the hearts of mice, the researchers determined that products of these reactive oxygen species modify proteins in the heart so that the immune system views them as a potential threat.

"The formation of these new targets is what we found that our T cells are robustly responding to," says Jay Ngwenyama, a postdoctoral scholar in Alcaide's lab and lead author on the study. "And this ultimately leads to inflammation that affects the heart."

The researchers confirmed that these modified proteins also appeared in the cardiac tissue of human patients whose hearts were failing.

Chronic inflammation can cause structural changes to the heart--the muscle can become enlarged or develop fibrous tissue, impeding its ability to pump blood efficiently and leading to further deterioration. But anti-inflammatory treatments or attempts to broadly target reactive oxygen species have yet to be successful, Ngwenyama says. They often end up interfering with other aspects of the immune system or necessary physiological processes.

With this improved understanding of how T cells are being activated in patients with heart disease, the researchers hope to develop more targeted treatments. They have already tested one possibility in mice: an agent that binds to the specific molecules altering cardiac proteins.

"We were actually able to prevent the inflammation and cardiac dysfunction that typically occur," Ngwenyama says. "So we're hoping that down the road this could have some significant implications in terms of treating humans for heart failure."