Interleukin-11 (IL-11), a member of the IL-6 cytokine family, plays a pivotal role in driving pulmonary inflammation, fibrosis, and cancer progression. As a distinct regulator, IL-11 exerts contrasting effects depending on the disease context. During acute inflammation, IL-11 maintains alveolar integrity, mitigates oxidative stress, and modulates immune responses. However, chronic IL-11 signaling promotes airway remodeling and fibrosis in diseases such as asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). We propose an ecological model in which IL-11 acts as a "keystone species" within interconnected pulmonary niches-epithelial, stromal, and immune cells-that collectively facilitate the transition from inflammation to fibrosis and ultimately to cancer. Targeted therapeutic strategies against IL-11 signaling are emerging, including neutralizing antibodies, receptor antagonists, engineered decoy ligands, and IL-11Rα-directed fusion toxins. Additionally, RNA interference (RNAi)-based approaches and small-molecule inhibitors targeting downstream IL-11 pathways (e.g., JAK/STAT3, MEK/ERK) have demonstrated substantial preclinical efficacy. This review underscores IL-11's critical role in pulmonary disease pathogenesis and highlights its potential as a therapeutic target. Further clinical validation and biomarker development are essential to translate these insights into personalized treatment strategies for diseases spanning inflammation, fibrosis, and cancer.
Yu et al. (Mon,) studied this question.
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