Interleukin 11 (IL11), a cytokine of the IL6 family, was initially misconstrued as a haematopoietic and cytoprotective factor, but recent research has corrected this view [4]. It signals via JAK/STAT3, ERK/P90RSK, LKB1/mTOR and GSK3β/SNAI1 pathways in autocrine and paracrine manners following tissue injury, activating mesenchymal transition of epithelial, stromal, and endothelial cells, which leads to inflammation, fibrosis, and impaired endogenous tissue repair [4]. Genetic models, such as KO or CKO mouse models, have been crucial in clarifying its role.

In various disease models, the importance of IL11 has been highlighted. In a bleomycin-induced pulmonary fibrosis mouse model, inhaled siRNA nanoparticles targeting IL11 inhibited lung fibrosis and improved pulmonary function, indicating its role in fibroblast differentiation and extracellular matrix deposition in the lung [1]. In kidney disease models, Il11 deletion or anti-IL11 antibody treatment reduced renal pathologies in acute kidney injury, and in a chronic kidney disease model, anti-IL11 therapy promoted renal parenchymal regeneration [2]. In preeclampsia models, PEGIL11 activated the placental inflammasome, causing inflammation, fibrosis, and hypertension in wild-type mice, and genetic loss of inflammasome components prevented some of these effects [3].

In conclusion, IL11 is a key cytokine involved in inflammation, fibrosis, and tissue repair processes. The use of KO/CKO mouse models has revealed its significance in diseases like pulmonary fibrosis, kidney diseases, and preeclampsia. Targeting IL11 signaling shows promise as a therapeutic approach for these and potentially other related diseases.