
In Australia, nearly 2% of the population will experience a heart attack or myocardial infarction (MI) during their lifetime. When the heart muscle is injured, it triggers acute inflammation, which is crucial for removing damaged tissues, repairing, and healing. However, excessive inflammation can cause further damage to the heart, increasing the risk of arrhythmias, heart failure, and hospitalisation. While medications and interventions can delay the onset of these cardiomyopathies, there is currently no effective treatment to minimise heart muscle damage post-heart attack to prevent their development. Many individuals who have experienced a heart attack continue to face long-term health issues or disabilities that significantly impact their quality of life.
Our team has discovered a novel mechanism that regulates inflammation. We have demonstrated that a redox enzyme controls the movement of immune cells to the site of injury, where they trigger inflammation. Importantly, inhibiting this enzyme's activity reduces immune cell movement, making it a promising therapeutic target for reducing acute inflammation. This project will use blood-vessel-on-a-chip assays and an animal model of heart attack to evaluate the effectiveness of targeting this redox enzyme in reducing acute inflammation and heart muscle damage.
In the short term, this project will provide insights into new strategies for controlling acute inflammation following a heart attack. In the long term, developing novel anti-inflammatory drugs that target this redox enzyme will enhance the recovery of heart injuries and reduce the risk of developing long-term cardiomyopathies.
Last updated26 May 2026