New research suggests that the stress of heart failure doesn’t just pass once the immediate crisis is over; it lingers, affecting the body’s ability to recover and leading to repeated health problems.
This phenomenon, identified in a recent study, shows how heart failure can leave a lasting imprint or “stress memory” in the body’s cells, particularly affecting the hematopoietic stem cells—those responsible for producing blood and immune cells.
These stem cells, located in the bone marrow, undergo changes in their DNA when stressed by heart failure. This modification impairs their ability to produce macrophages, a type of immune cell critical for protecting the heart and other organs.
The research pinpointed a key issue: a signaling pathway in these cells, known as transforming growth factor beta (TGF-β), becomes suppressed during heart failure.
This suppression hampers the production of effective macrophages, thus weakening the body’s defense against recurring heart issues.
The implications of this research are profound. By boosting TGF-β levels, it might be possible to treat or even prevent recurrent heart failure.
Furthermore, monitoring the build-up of stress memory in these stem cells could provide an early warning system for heart failure before it reoccurs.
This study aligns with global efforts to improve health outcomes, as emphasized by the United Nations’ Sustainable Development Goals, which aim for enhanced well-being and longer life expectancy.
Despite progress in public health leading to a projected increase in life expectancy by about 4.5 years by 2050, heart disease remains the leading cause of death worldwide, affecting an estimated 26 million people.
Researchers, particularly in Japan, are keen to understand why heart failure and its associated complications, like kidney and muscle disorders, tend to recur.
Their findings, published in the journal Science Immunology, suggest that the accumulation of stress during an episode of heart failure is a key driver of these repeated health issues.
The team conducted their research using mice, observing how heart failure induced lasting chemical changes to the DNA of the hematopoietic stem cells.
They discovered that the altered stem cells continued to produce poorly functioning immune cells long after the initial heart failure event.
Even more striking, when they transplanted the affected bone marrow into healthy mice, these mice too started showing signs of heart failure and other organ damage.
The term “stress memory” aptly describes how the trauma of heart failure persists within the body, continually influencing health. The stress induced by heart failure is notably impactful, potentially setting the stage for a cycle of recurring health problems.
However, there’s optimism in the air. Identifying the changes in the TGF-β signaling pathway opens new doors for innovative treatments.
For instance, supplementing with active TGF-β or correcting the altered DNA in hematopoietic stem cells could potentially erase the harmful stress memory, offering a fresh therapeutic approach.
As research advances, the next steps involve developing methods to detect and counteract the accumulation of stress memory in humans.
This could not only prevent the recurrence of heart failure but also intercept the condition before it fully manifests, marking a significant stride towards better heart health management.
If you care about heart health, please read studies that yogurt may help lower the death risks in heart disease, and coconut sugar could help reduce artery stiffness.
For more information about health, please see recent studies that Vitamin D deficiency can increase heart disease risk, and results showing vitamin B6 linked to lower death risk in heart disease.
The research findings can be found in Science Immunology.
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