Rogue DNA Tied to Heart Failure

DNA mistakenly activates immune system

(RxWiki News) The heart's own "rogue DNA" appears to play a role in the development of heart failure. A new study has found that the heart's own cells mistakenly activate the immune system, contributing to heart failure.

During heart failure, immune cells cells invade the heart. This process, called inflammation, which ultimately leads to a less efficient heart with less pumping ability in the case of heart failure, can be caused by the body's own DNA.

"Don't smoke to protect your heart."

Professor Kinya Otsu, study leader and British Heart Federation Professor of Cardiology at King's College London, made the finding by studying heart inflammation caused by the body's own DNA in mice.

During the study researchers found that DNA escapes when a natural process to break down damaged cell components becomes less efficient. A common reason for the inefficiency is stress, such as during heart failure.

Rogue DNA comes from the mitochondria, structures in heart cells that produce energy. Mitochondrial DNA triggers inflammation because it resembles DNA from bacteria, and this sets off an immune cells receptor known as the Toll-like Receptor 9 (TLR9). This is particularly interesting since mitochondria is believed to have evolved from bacteria over a billion years ago.

In the current study researchers found that the human immune system still appears to recognize this archaic bacterial fingerprint in mitochondrial DNA, which causes an immune response.

"When mitochondria are damaged by stress, such as during heart failure, they become a problem because their DNA still retains an ancient bacterial fingerprint that mobilizes the body's defenses," Otsu said.

"We previously showed that damaged mitochondria build-up during heart failure, when the natural processes of cell breakdown become less effective. Now we've shown that the DNA fingerprint that we retain in our mitochondria causes our own immune system to turn against us."

The study was published April 25 in journal Nature.

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Review Date: 
April 24, 2012