A recent study by researchers at the Smidt Heart Institute at Cedars-Sinai has unveiled a groundbreaking technique that enhances the body’s production of anti-inflammatory cells, facilitating rapid healing from heart attacks in mice.
This promising approach could potentially be adapted for human treatment, offering new hope for repairing heart muscle damage post-heart attack and addressing various inflammatory disorders.
Published in the peer-reviewed Journal of Clinical Investigation, the study highlights a significant challenge in heart attack recovery: uncontrolled inflammation.
Each year, over 800,000 individuals in the U.S. suffer heart attacks, often leading to tissue damage due to an overactive immune response that exacerbates inflammation and increases the risk of heart failure.
To combat this issue, the Cedars-Sinai team focused on boosting the supply of regulatory T-cells (Tregs), which play a crucial role in modulating immune responses and preventing excessive inflammation.
Traditional methods of extracting and expanding Tregs are too slow for acute situations like heart attacks. Instead, researchers developed a method that stimulates the body to produce its own Tregs through infusions of extracellular vesicles containing an RNA molecule called BCYRN1.
Laboratory experiments demonstrated that mice treated with these vesicles shortly after experiencing heart attacks exhibited increased Treg levels in their hearts, resulting in reduced cardiac tissue damage and inflammation compared to untreated mice. Notably, these treated mice also maintained better heart function.
The extracellular vesicles used in this study were derived from cardiosphere-derived cells (CDCs), which naturally contain high levels of BCYRN1.
This research underscores the potential of using extracellular vesicles as a delivery system for therapeutic benefits, paving the way for future clinical applications in heart disease management and beyond.
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