The role of the XIIIA clotting factor in heart scarring

The role of Coagulation Factor XIII-A in myocardial tissue repair and cardiac function

After a heart attack the lack of oxygen to the heart muscle triggers a process called fibrosis, where scar tissue build-up prevents the heart from beating normally. Fibrosis plays an important part in heart failure development and also occurs in other conditions such as diabetes. Over the past five years a University of Leeds team have found a link between fibrosis and a protein involved in blood clotting. This project, led by Professor Peter Grant, will clarify the influence of the protein, factor XIIIA, on heart scarring. Factor XIIIA helps to stabilise the protein fibrin, which in turn stabilises blood clots. Mice without factor XIIIA develop heart scarring much more easily than normal mice, even in the absence of heart damage. This has led the scientists to propose that the factor is important in day-to-day background heart muscle repair, as well as having a role in reducing heart scarring after a heart attack. Another important possibility raised by this discovery is that existing anti-clotting drugs given to patients after a heart attack, which target Factor XIIIA, could have a long-term effect on the level of scarring in the heart. Over the next five years, Professor Grant aims to work out the ways in which factor XIIIA helps reduce heart scarring, and in particular how it could work alongside another protein called transglutaminase 2 to perform this role. This research is important to better understand the process of heart muscle repair. It’s also important to make sure that future anti-clotting drugs do not inadvertently increase fibrosis in the heart by undermining factor XIIIA’s ability to reduce heart muscle scarring.