Analysis of the defensive properties of two anti-inflammatory molecules, transforming growth factor-beta1 (TGF 1) and Heligmosomoides polygyrus TGM (HpTGM), after a heart attack showed that both proteins decreased the inflammatory response in the damaged heart and reduced the formation of mature scar tissue. Researchers report that the use of anti-inflammatory treatment for patients following a heart attack is a promising possibility that warrants further research.
Research into the protective effects of two anti-inflammatory molecules, transforming growth factor-beta1 (TGFβ1) and Heligmosomoides polygyrus rnrn TGM (HpTGM) discovered that both proteins reduced the inflammation in the damaged heart and decreased the formation of scar tissue. Treating patients with anti-inflammatory therapy after a heart attack is an exciting possibility that should be further studied, according to researchers in The American Journal of Pathology published by Elsevier.
Patients who suffer from acute heart attacks (ST elevation myocardial infarction, or STEMI) have a high chance of survival if they receive prompt reopening of the blocked coronary artery (coronary reperfusion) in specialized clinical centers.The survival rates and treatment for heart attacks have improved significantly, but many patients still develop heart failure. The long-term outcomes for these patients are determined by the extent of damage to their heart tissue. Dr. Helen M. Arthur, the lead researcher at Newcastle University, explains that while restoring blood flow to the heart after a heart attack is a common treatment, the body’s inflammatory response to repair the damaged tissue can actually cause more harm by causing additional loss of healthy heart muscle.The researchers wanted to find out if TGFβ1 could help protect the heart from further damage after a heart attack. They found that higher levels of TGFβ1 in the blood of patients who had a heart attack were linked to a smaller area of damage to the heart muscle three months later. They then tested this further on mice with heart attacks to see if TGFβ1 could help protect their hearts.The researchers examined the effects of TGFβ1, a protein released in the body in response to tissue injury, and its mimic HpTGM, a protein produced by a parasitic worm to evade the immune response. They found that delivering either of these proteins intravascularly reduced the inflammatory response within the heart and decreased the extent of heart injury, as shown by reduced scar size. The researchers were surprised to discover that TGFβ1 and HpTGM had almost identical beneficial effects, despite being evolutionarily unrelated.Both molecules interact with cells in a similar way by activating the same signaling pathway. The anti-inflammatory therapy was administered at the time of reperfusion, which is a clinically useful time for intervention in humans.
Investigators believe that the positive effects could be attributed to the protective impact of these molecules on endothelial cells, which line the blood vessels and help regulate the movement of proinflammatory white blood cells from the circulation into the injured tissue. TGFβ1 is known for its anti-inflammatory properties, while HpTGM mimics parasites.The Maizels laboratory at the University of Glasgow has discovered that the delivery of HpTGM has significant potential for clinical use. Their research has demonstrated that HpTGM has anti-inflammatory effects on mouse models of colitis and airway inflammation. This is due to the parasite’s ability to suppress the immune response. Dr. Arthur’s study has shown that delivering HpTGM during coronary artery reperfusion can reduce the proinflammatory response of coronary endothelial cells, decrease cardiac injury, and improve myocardial salvage. This ultimately results in reduced scar size and improved prospects for patients.The use of HpTGM as a therapy for reducing inflammation in heart attack patients is an exciting prospect that requires further studies to determine its potential long-term benefits for cardiac function.
