The regulation of inflammation in ventricular remodelling after myocardial infarction

After a heart attack, the body’s own inflammatory cells can worsen heart damage, driving the heart toward failure. This project investigates why that happens and how to stop it. Heart failure after a heart attack remains a major cause of illness and death, even with current treatments. The problem is inflammation—specifically, the flood of monocytes and macrophages that rush to the injured heart. While some inflammation is needed for healing, too much of it scars the heart muscle and impairs its pumping ability. Researchers know that a molecule called Nrf2 can dampen this harmful inflammation, but they do not yet understand exactly how it controls the behaviour of those key immune cells. This is fundamental science. The team will manipulate Nrf2 in animal models to trace the molecular signals that turn protective inflammation into destructive inflammation. If they can map those pathways, they may identify new drug targets for preventing heart failure after a heart attack. Similar fundamental work on immune signalling has already led to anti-inflammatory therapies for arthritis and other conditions. A deeper understanding here could eventually yield treatments that spare patients the progressive decline of heart failure—a condition that currently affects hundreds of thousands of people in the UK alone.