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In a significant breakthrough, research investigating the protective effects of two anti-inflammatory molecules, transforming growth factor-beta1 (TGFβ1) and Heligmosomoides polygyrus TGM (HpTGM), following heart attacks, has unveiled promising results. Both proteins were found to significantly reduce the inflammatory response within the injured heart and diminish mature scarring, offering hope for potential anti-inflammatory therapy in treating patients following acute myocardial infarction.
Published in The American Journal of Pathology by Elsevier, the study sheds light on the potential of anti-inflammatory interventions to mitigate the damaging effects of heart attacks, paving the way for further translational studies.
Lead investigator Helen M. Arthur, PhD, from Newcastle University’s Biosciences Institute, highlighted the critical need for interventions to minimize additional damage to the heart tissue beyond the ischemic damage caused by the heart attack itself. Despite timely coronary reperfusion being standard therapy for patients with acute heart attacks (ST elevation myocardial infarction, or STEMI), progression to heart failure remains a significant clinical challenge, underscoring the importance of exploring novel therapeutic avenues.
The research team observed that levels of TGFβ1, an essential anti-inflammatory protein, in the blood of STEMI patients 24 hours after reperfusion correlated with a reduction in infarct size after three months. Further investigations in a mouse model of a heart attack revealed that intravascular delivery of either TGFβ1 or its mimic HpTGM resulted in reduced inflammatory response within the heart and, importantly, decreased extent of heart injury, evidenced by reduced mature scar size.
Surprisingly, both TGFβ1 and HpTGM demonstrated almost identical beneficial effects despite being evolutionarily unrelated. Their interaction with cells activated the same signaling pathway, indicating their potential clinical utility.
The study attributed the protective outcomes to the molecules’ effects on endothelial cells, the lining of blood vessels crucial for regulating the entry of proinflammatory white blood cells into the injured tissue. TGFβ1’s well-established anti-inflammatory properties, coupled with HpTGM’s clinical potential as a parasitomimetic, present exciting prospects for future therapeutic interventions.
Dr. Arthur emphasized the significance of these findings, stating that HpTGM’s use as an anti-inflammatory therapy in heart attack patients holds promise for increased myocardial salvage, reduced scar size, and improved long-term cardiac function. The study underscores the need for further translational studies to explore the full potential of HpTGM and TGFβ1 as therapeutic interventions in treating heart attack patients.
