Active Heart, Stroke & Blood Lungs & Breathing

Exploring the role of interleukin-11 in patients with atrial fibrillation

Funder BHF Charity-funded
Recipient organisation University of Oxford
Funding £275K
Period Jul 2025 — Nov 2027

In plain English

AI plain-English summary

A protein called interleukin-11 is elevated in the blood and heart tissue of people with atrial fibrillation, a common heart rhythm disorder that raises the risk of stroke. Atrial fibrillation affects millions of people worldwide. Current treatments focus on controlling the heart's electrical activity, but they do not address the underlying structural damage—specifically, fibrosis, or scarring of the heart's upper chambers. This scarring makes the arrhythmia worse and harder to treat. No drugs exist to prevent or reverse it. The researchers suspect that interleukin-11, which is known to drive fibrosis in other heart conditions, may also be responsible for the scarring seen in atrial fibrillation. This project will track where the protein comes from, how its levels change over time, and whether it correlates with patient outcomes. It will also test how the protein affects human atrial fibroblast cells in the lab. If the link holds, interleukin-11 could become a target for drugs that prevent atrial scarring—potentially offering a new treatment avenue for a condition that currently has none. The work is fundamental science: it aims to clarify a biological mechanism, not to test a therapy. But understanding that mechanism is the necessary first step toward developing one.

View original technical description
Atrial fibrillation (AF), the commonest cardiac arrhythmia, is a leading cause of stroke and an important contributor to human mortality and morbidity. Treatment remains challenging due to atrial electrical and structural remodelling (fibrosis). While therapies target electrical remodelling, no effective therapies exist for atrial fibrosis. The cytokine interleukin(IL)-11 (IL11), a member of IL6 cytokine family, is reported to play a role in cardiac fibrogenesis. However, its role in AF and atrial structural remodelling is unclear. Our pilot work found increased atrial gene expression, and coronary-sinus and circulating IL11 levels in patients with paroxysmal-AF compared to non-AF controls. IL11 positively correlates with age, AF major risk factor. We hypothesise that IL11 may play a role in AF pathogenesis, and aim to assess (i) IL11 sources (circulating, myocardium-secreted and atrial-cellular) and temporal changes in circulating IL11, (ii) association of IL11 levels with clinical outcomes/parameters, and (iii) IL11-mediated effects on human atrial fibroblast functions. These will be explored in the context of potential synergy/interplay with IL6 in human atrial tissue/cells and, peripheral and coronary sinus blood samples using complex molecular/cellular biology and high throughput approaches. This project will provide new insights into the role of IL11/IL6 in human AF and AF-associated structural remodelling.

View the original record at the funder ↗

Researchers

Svetlana Reilly (EPMC Awardee)

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Original classification

None

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