AsianScientist (Apr. 30, 2012) – DNA from the heart’s own cells may play a role in heart failure by mistakenly activating the body’s immune system, researchers have found.
Scientists from King’s College London, U.K., and Osaka University Medical School, Japan, show that ‘rogue DNA’ can kick start the body’s natural response to infection, contributing to the process of heart failure.
During heart failure immune cells invade the heart, a process called inflammation which is normally caused by bacterial or viral infection. The process makes heart muscle less efficient, reducing its ability to pump blood around the body.
The study, published in the journal Nature, shows in mice that inflammation in the heart can be caused by the body’s own DNA. The DNA escapes when a natural process to break down damaged cell components, called autophagy, becomes less efficient, which sometimes happens when cells are under stress such as during heart failure.
The problem DNA comes from mitochondria, energy-generating structures in heart cells which resemble DNA from bacteria. These DNA trigger a receptor in immune cells called Toll-like Receptor 9 (TLR9).
Mitochondria in our cells are believed to have evolved from bacteria more than 1.5 billion years ago, and this study shows that the human immune system still recognizes the bacterial fingerprint in mitochondrial DNA, triggering a response from the immune system.
“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,” said Professor Kinya Otsu who led the study.
As heart cells are packed with mitochondria, which provide the power the heart needs to pump blood around the body, understanding how mitochondrial DNA causes part of the problem during heart failure may lead to future treatments for heart failure, the authors say.
The article can be found at: Oka T et al. (2012) Mitochondrial DNA That Escapes from Autophagy Causes Inflammation and Heart Failure.
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Source: British Heart Foundation.
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