Source: University of California San Diego
Summary: Researchers have found that the immune system plays a surprising role in the after-effects of heart attacks. The findings could lead to new therapeutic strategies for cardiac diseases.
Ischemic heart disease also called as coronary artery disease (CAD) is the most common cause of death in the world. CAD ultimately can lead to heart attack. During a heart attack, the heart cells die, which prompts the immune cells to enter the dead tissue, cell debris and stabilize the heart wall. To check the stimulation of immune system by the dying cells of the heart, researchers from University of California San Diego, Massachusetts General Hospital, Brigham and Women’s Hospital, Harvard Medical School and the University of Massachusetts looked inside many cardiac immune cells and mapped their transcriptomes individually by using single-cell RNA-Seq. This led to the finding that after a heart attack, dying cells DNA masquerades as a virus and stimulates an old antiviral program, the type 1 interferon response in specialized immune cells and the researchers named these “interferon-inducible cells (IFNICs).” The findings were published in the journal Nature Medicine.
When the interferon response is blocked either genetically or with a neutralizing antibody after the heart attack, there was less inflammation, less heart dysfunction, and improved survival. Blocking antiviral responses improved survival rates from 60% to 95% in mice. By using single-cell RNA-seq (combines microfluidic nanoliter droplet reactors with single cell barcoding). The researchers were able to examine every gene expression in over 4000 cardiac immune cells and found the specialized IFNIC population of responsible cells. These findings reveal a new potential therapeutic strategy to avoid heart attacks from progressing to heart failure in patients.
Kevin King said, “We are interested to learn whether interferons contribute to adverse cardiovascular outcomes after heart attacks in humans.”
More Information: Kevin R King et al, “IRF3 and type I interferons fuel a fatal response to myocardial infarction”, Nature Medicine (2017).