Cardiovascular disease is the leading cause of death worldwide, with a major contribution from myocardial infarction (MI), also known as a heart attack. Inflammation and ensuing fibrotic scarring on the heart are critical determinants of outcome post heart attack.
A key, but elusive, therapeutic goal for scientists is to modulate inflammation and scarring, while enhancing normal healing. The cardiac scar that forms in the human heart after heart attack is permanent, so the heart is not able to pump as efficiently as before injury, eventually leading to heart failure. However, remarkably, some fish and neonatal mice do not scar after injury, but instead regenerate functional heart tissue. Inflammatory cells are essential for this regeneration, though their precise role is not understood.
DPAG's Associate Professor Mathilda Mommersteeg and Professor Paul Riley, together with Professor Robin Choudhury from the Radcliffe Department of Medicine, have received funding from the Chan Zuckerberg Foundation to study the role of inflammatory cells in regenerative versus non-regenerative models post-myocardial infarction using single cell RNA sequencing (SC-Seq) and computational biology.
This grant is part of a new Initiative supporting 29 interdisciplinary teams to build a network of researchers exploring emerging ideas on the role of inflammation in disease. The teams will carry out two-year pilot projects focused on tissue-level inflammatory processes in diverse tissues and disease states.
Head of Science at the Chan Zuckerberg Initiative (CZI) Cori Bargmann said: "Knowing more about inflammation at the level of affected cells and tissues will increase our understanding of many diseases and improve our ability to cure, prevent, or manage them."
More information on the CZI and its funded projects can be found here.