Health
Understanding a broken heart | ScienceDaily
The stress of heart failure appears to be stored in the body and lead to recurrence of heart failure, along with other associated health problems, according to a new study. Researchers found that heart failure leaves a “stress memory” in the form of changes in DNA modifications in hematopoietic stem cells involved in generating blood and immune cells called macrophages. These immune cells play a key role in protecting heart health. However, during heart failure, a key signaling pathway called transforming growth factor beta (TGF-β) in hematopoietic stem cells (a chain of molecules that relay signals within cells) was suppressed, negatively affecting the generation of macrophages. Improving TGF-β levels could be a new way to treat recurrent heart failure, while detecting accumulating stress memories could provide an early warning system before it happens.
Healthier lives and improved well-being are one of the United Nations' Sustainable Development Goals. On a bright side, recent studies predict that global life expectancy will increase by about 4.5 years by 2050, thanks in large part to public health efforts to prevent diseases such as cardiovascular disease and improve survival rates. However, heart disease remains the number one cause of death worldwide, with an estimated 26 million people suffering from heart failure.
Once heart failure has set in, it tends to recur along with other health problems such as kidney and muscle problems, and researchers in Japan wanted to understand what causes this recurrence and the deterioration of other organs, and whether it could be prevented.
“Based on our research, we hypothesized that the stress experienced during heart failure accumulates in the body, particularly in hematopoietic stem cells, which lead to recurrence,” explains Katsuhito Fujio, a professor at the Graduate School of Medicine at the University of Tokyo. Hematopoietic stem cells are found in the bone marrow and are the source of blood cells and a type of immune cell called macrophages, which help protect the health of the heart.
By studying mice with heart failure, the researchers found evidence that stress imprinted the epigenome, or caused chemical changes in the mice's DNA: Transforming growth factor beta, a key signaling pathway involved in regulating many cellular processes, was suppressed in hematopoietic stem cells from mice with heart failure, leading to the generation of dysfunctional immune cells.
The changes persisted for so long that when the team transplanted bone marrow from the mice with heart failure into healthy mice, they found that the stem cells continued to produce dysfunctional immune cells — the latter mice later developed heart failure and were more susceptible to organ damage.
“Because the stress caused by heart failure is stored for a long time and continues to affect the entire body, we named this phenomenon stress memory. Although various other types of stress may also be imprinted on this stress memory, we believe that the stress caused by heart failure is particularly large,” Fujio said.
The good news is that identifying and understanding these changes in the TGF-β signaling pathway opens new avenues for future treatments. “We may be able to come up with entirely new therapies to prevent this stress memory from building up during hospitalization for heart failure,” Fujio says. “In animals with heart failure, supplementation with additional active TGF-β has been shown to be a potential treatment. Modifying the epigenome of hematopoietic stem cells may also be a way to reduce stress memory.”
Now that the stress memory buildup has been identified, the team hopes to develop a system that can detect and prevent it in humans, with the long-term goal not just to prevent the recurrence of heart failure, but to be able to detect it before the condition fully progresses.
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