Non-apoptotic cell death in heart failure

Heart muscle cells in failing hearts are dying in a way that triggers harmful inflammation, and researchers want to stop it. Heart failure affects nearly one million people in the UK. Current treatments focus on managing symptoms, not on preventing the cell death that drives the condition. The team previously discovered that when damaged mitochondria—the cell’s power plants—are not properly cleared, their DNA leaks out and provokes an inflammatory response that kills more cells. They also identified a protein, Bcl2-like protein 13, that normally tags damaged mitochondria for disposal. Separately, they found that the speed at which cells break down inflammatory messenger RNA may determine how long inflammation lasts. This project asks whether boosting the cell’s ability to degrade both mitochondrial DNA and inflammatory mRNA could halt the cycle of inflammation and cell death. The researchers will map the molecular machinery behind these clean-up processes, test whether their activity predicts disease severity, and explore whether tweaking them could become a treatment. If successful, this fundamental science could reveal entirely new drug targets for heart failure—not just managing symptoms, but addressing the root cause of tissue damage.