High Mobility Group Protein B1 Mediates The Role Of The Neutrophil Extracellular Traps In The Progression Of Acute Myocardial Infarction
When someone experiences a heart attack, a type of immune cell called neutrophils can release sticky, web-like structures known as neutrophil extracellular traps, or NETs. These NETs, while part of the body’s defense system, can unfortunately contribute to further damage in the heart by increasing inflammation and leading to scar tissue formation. Recent research has shed light on a key protein, High Mobility Group Protein B1 (HMGB1), that acts as a major driver in this process.
Scientists investigated how this protein influences NET formation in patients who suffered a severe type of heart attack and in animal models. They found that higher levels of HMGB1 were present in patients, and in mice, this protein actively encouraged the creation of NETs. This, in turn, intensified the inflammatory response and the development of fibrosis, which is the thickening and scarring of heart tissue.
Crucially, the study demonstrated that by blocking HMGB1 or by breaking down NETs, it was possible to reduce their harmful effects and improve heart function. These findings suggest that targeting this specific pathway could offer a promising new approach to developing treatments that limit heart damage after a heart attack and potentially address issues related to cellular aging in the context of heart injury.
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