After a heart attack (myocardial infarction), the body's inflammatory response can do as much damage as the event itself. This project investigates how activation of the NLRP3–Gasdermin D axis — a key innate immune pathway — drives excessive inflammation and impairs the heart's ability to recover following injury.
By dissecting the molecular mechanisms linking inflammasome activation, Gasdermin D–mediated pore formation and inflammatory cell death (pyroptosis), we aim to identify the key drivers of post-infarct cardiac dysfunction and adverse remodelling. Using a combination of in vivo and cellular models, this research will determine whether targeted modulation of this pathway can limit damaging inflammation, preserve viable heart muscle and improve cardiac function after a heart attack.
This project offers students and postdoctoral researchers the opportunity to develop deep expertise in inflammasome biology — with direct relevance to developing new therapeutic strategies for improving outcomes after myocardial infarction.