The effect of hyperglycaemia upon cardiac innate immune cell immunometabolism following myocardial infarction

Diabetes is associated with adverse clinical outcomes following myocardial infarction (MI) as well as greater myocardial fibrosis and impaired systolic and diastolic function. The mechanisms behind these effects are poorly understood and there are no specific immunomodulatory therapeutic options for affected patients. The local innate immune response following MI controls cardiac remodelling and could in principle be therapeutically targeted in the days following the event.  Furthermore, metabolic reprogramming towards glycolysis in activated monocytes/macrophages is essential for their polarization to an inflammatory phenotype and can be assessed non-invasively following MI with hyperpolarized [1-¹³C]pyruvate MRI.

This BHF CRE pilot project will develop methods and seek discovery data in this area, to underpin the design of future studies on the effect of diabetic hyperglycaemia on myocardial immune cell immunometabolic function in mice. The research has clear potential links to future human experiments using hyperpolarized MRI to study immune responses following MI.

This project may highlight new therapeutic targets in myocardial infarction in patients with diabetes.

The project is led by Dr Andrew Lewis, Clinical Researcher, OCMR, Oxford BHF CRE