Their regulation of fibroblasts, CD8+ T cells, neutrophils, and other immune cells underscores their potential as therapeutic targets for mitigating disease progression, emphasizing the critical roles of NEAT1, MALAT1, HOTAIR, MEG3, GAS5, and TUG1 in the pathogenesis and progression of COPD (Figure 4B). This evidence concerns the gene HOTAIR and chronic obstructive pulmonary disease.