TGFβ-signalling is a major driver of pathological fibrosis, which accompanies most heart disease. Targeting TGFβ therapeutically has proven difficult due to its pleiotropic role in the body, and thus, strategies to target specific TGFβ pathways are warranted to develop new treatment for cardiac fibrosis. Together with colleagues, PhD student Karoline Rypdal in the group of Ida Lunde, found that the extracellular matrix protein, ADAMTSL2, was increased in failing hearts of patients and mice. By over-expressing ADAMTSL2 in cultures of cardiac fibroblasts, they discovered that ADAMTSL2 inhibited TGFβ-signalling and had an anti-fibrotic effect on cardiac fibroblast phenotype, preventing the fibroblasts from transdifferentiating into pro-fibrotic myofibroblasts. These findings indicate a potential novel target for preventing pathological TGFβ-signalling in heart failure.