| Description |
This study investigates the role of IL6-AS1, a highly expressed long non-coding RNA (lncRNA), in chronic obstructive pulmonary disease (COPD). An adeno-associated virus (AAV) was used to induce the expression of IL6-AS1 in mice, and they were exposed to cigarette smoke to establish a COPD model. Our findings indicate that the upregulation of IL6-AS1 in fibroblasts enhances the interaction between the S100A9 protein and the AGER and TLR4 receptors on lung macrophages, thereby exacerbating inflammatory responses. These findings suggest that IL6-AS1 may play a role in facilitating the crosstalk between fibroblasts and macrophages, leading to increased pulmonary inflammation. Mendelian randomization analysis further suggests a potential shared causal variant between IL6-AS1 and COPD. Taken together, this investigation provides valuable insights into the function of IL6-AS1 and its potential implications for the pathogenesis and therapeutic strategies in COPD. |