Newcastle University’s compelling new research shows anti-inflammatory molecules reduce the scar size on the heart, leading to improved chances of long-term cardiac function
A study done by the Newcastle University team discovered a correlation between a decrease in infarct size after three months and the concentrations of TGFβ1, a significant anti-inflammatory protein, in the blood of STEMI patients 24 hours after reperfusion. To explore this further, they tested the protective effects of TGFβ1, a protein known to be secreted in the body in response to tissue injury, and its imitation, HpTGM, using a well-established mouse model of a heart attack.
Two proteins have been found to lessen scarring and the inflammatory response in the damaged heart because of studies on the preventive benefits of two anti-inflammatory molecules after a heart attack.
Two anti-inflammatory molecules that have been identified to be helpful in therapy are Heligmosomoidespolygyrus TGM (HpTGM) and Transforming Growth Factor-beta1 (TGFβ1). When patients with acute heart attacks (also known as STEMIs) receive prompt reopening of the blocked coronary artery (coronary reperfusion) in specialised healthcare facilities, their chances of survival increase significantly. But even with significant advancements in medicine, the development of heart failure remains a significant clinical issue.
Professor Helen Arthur, Professor of Cardiovascular Biology at Newcastle University, said, “Coronary reperfusion after STEMI is standard therapy to salvage ischemic heart muscle. However, evidence suggests that the subsequent inflammatory response that the body initiates to repair the damaged heart tissue can also cause further loss of viable heart muscle and the more muscle that is lost the greater the risk of subsequent progression to heart failure. The reason for this study was to investigate the potential protective effects of TGFβ1 as a possible intervention to minimize this additional damage to the heart beyond the ischemic damage caused by the heart attack itself.”
The investigators were surprised
The protein, generated by a parasitic worm, aids in evading the immune system, allowing the worm to survive within the gut’s tissue lining. Introducing either of these naturally occurring anti-inflammatory proteins into the bloodstream decreased harmful inflammation in the heart and notably reduced heart damage, as indicated by smaller scar formation.
The researchers were surprised to observe similar positive effects from both TGFβ1 and HpTGM treatments, despite their evolutionary differences. Both molecules interacted with cells comparably, activating the same signaling pathway. Administering the anti-inflammatory treatment at the time of reperfusion, a clinically relevant intervention period in humans, yielded beneficial results.
The protective impact of these molecules on endothelial cells, which line blood vessels and regulate the movement of pro-inflammatory white blood cells from circulation into injured tissue, likely contributed to the favorable outcomes.
While TGFβ1 is known for its anti-inflammatory properties, HpTGM mimics parasites and holds promising clinical potential. Recent research at the University of Glasgow’s Maizels lab has demonstrated that delivering HpTGM significantly reduces inflammation in mouse models of colitis or airway inflammation, leveraging a product evolved by parasites to suppress immune responses.
Prof Arthur added, “The current study shows that exogenous delivery of HpTGM at the time of coronary artery reperfusion dampens the proinflammatory response of coronary endothelial cells and reduces cardiac injury, leading to increased myocardial salvage and reduced scar size, with the corollary of improved prospects for long-term cardiac function. The use of HpTGM as an anti-inflammatory therapy in treating heart attack patients is an exciting prospect that requires further translational studies.”
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