Queen Mary researchers identify new blood vessel cells linked to liver fibrosis

8 October 2026

The study, published in JCI Insight and led by PhD student Christina Gkantsinikoudi and Dr Neil Dufton at Queen Mary’s William Harvey Research Institute (WHRI), identified what the researchers have termed ‘fibrosis-associated endothelial cells’ (FAEC).

The paper is a collaborative multicentre project involving Dr Dufton’s group at the WHRI, together with research groups led by Professor William Alazawi at Queen Mary’s Blizard Institute, Professor Karen Hanley-Piper at the University of Manchester and Professor Johnathan Fallowfield at the University of Edinburgh.

The cells appear early during liver injury, before visible signs of severe fibrosis develop. This suggests they could provide an early indicator of disease progression and potentially offer new targets for treatment.

Endothelial cells line the body's blood vessels and play an important role in maintaining healthy tissues. They are highly adaptable and can change their behaviour in response to injury and disease. During chronic disease, however, repeated damage can cause them to adopt harmful characteristics and contribute to tissue scarring, known as fibrosis.

The researchers wanted to understand why some blood vessels in the liver appear more susceptible to injury than others, and how endothelial cells change as liver fibrosis develops.

Using advanced imaging, full-spectrum flow cytometry and genetic profiling, the team characterised different populations of endothelial cells in models of liver fibrosis and samples from patients with metabolic dysfunction-associated steatotic liver disease (MASLD).

Their analysis revealed distinct populations of FAEC, demonstrating the diversity of endothelial cells during liver disease. The researchers believe this is the first time full-spectrum flow cytometry has been used to characterise different endothelial cell populations in this way.

One of the most striking findings was the identification of FAEC expressing TAGLN, a protein more commonly associated with cells involved in forming scar tissue.

TAGLN-positive FAEC were identified in liver samples from patients with MASLD, while higher levels of TAGLN were associated with poorer outcomes across different stages of liver disease.

Dr Neil Dufton, Senior Lecturer in Inflammatory Sciences at Queen Mary University of London, said: “What was really striking was how diverse and adaptable endothelial cells are. By using full-spectrum flow cytometry, we were able to identify different subpopulations of endothelial cells that appear during liver injury and fibrosis.”

MASLD affects millions of people worldwide and can cause progressive liver damage in some patients. Currently, it is difficult to identify which people with MASLD will go on to develop significant liver fibrosis, which is strongly associated with poorer health outcomes.

The findings suggest that TAGLN-positive FAEC could help identify patients at higher risk of disease progression earlier in the course of liver disease.

The team is now investigating why a particular population of TAGLN-positive FAEC appears to promote fibrosis in the liver, and whether these cells can be selectively targeted.

Dr Dufton said: “We are now trying to understand why TAGLN-positive FAEC appear to drive fibrosis in the liver. If we can find ways to selectively target these cells, it could open up new opportunities to prevent or potentially reverse tissue damage and fibrosis.”