Researchers at Massachusetts General Hospital have identified a potential path to treating atrial fibrillation by focusing on immune cells. The findings were reported in a study published in Science and highlight a new direction for therapy in this common heart rhythm disorder.
Atrial fibrillation is the most frequent heart rhythm problem, marked by rapid and irregular beats that raise the risk of stroke and heart failure. The study examined single cells from atrial tissue taken from both healthy individuals and people with arrhythmia, revealing that macrophages, a type of immune cell, proliferated more in the atrium during arrhythmia than any other cell type in the affected tissue.
Experiments conducted in mice showed that these macrophages contribute to atrial inflammation and scar formation, which disrupt the electrical signals between heart cells and sustain the irregular rhythm characteristic of atrial fibrillation.
When researchers looked at gene activity, they found heightened activity of the SPP1 gene in both human and mouse cardiac macrophages. This gene drives the production of osteopontin, a protein linked to tissue scarring during arrhythmia. In mice lacking osteopontin, the number of atrial macrophages declined, suggesting a direct link between this protein and the development of the condition.
From these observations, the researchers concluded that future drugs for atrial fibrillation could target atrial macrophages or inhibit osteopontin to reduce inflammation and scarring in the heart tissue, thereby improving electrical conduction and reducing rhythm disruption.
The authors emphasized that the study lays a foundation for immunomodulatory approaches to atrial fibrillation and noted ongoing efforts to translate these insights into several strategic therapies aimed at modulating the immune response within the atria.
These findings represent a shift toward understanding atrial fibrillation through the lens of immune system involvement, offering a potential complement or alternative to existing rhythm-control strategies. Scientists stress that while the data are promising, further work is needed to validate targets, assess safety, and determine how such therapies might be integrated with current treatments in humans, including anticoagulation and rhythm management approaches.
The research team also highlighted the importance of exploring how macrophages interact with cardiac tissue during arrhythmia, as such interactions may reveal additional targets for intervention. By characterizing the cellular and genetic signals at play, the study contributes to a broader effort to map the immune components that influence heart rhythm disorders and to develop therapies that can modulate these processes with precision.
Overall, the work from Massachusetts General Hospital adds a critical piece to the puzzle of atrial fibrillation. It points toward a future where managing the condition could involve dampening specific immune pathways in the heart, rather than focusing solely on controlling the electrical symptoms or using broad anti-inflammatory strategies. This evolving approach holds promise for more targeted, potentially safer treatments that address the root tissue changes driving the abnormal rhythm.
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