This study established a co-expression network based on TGF-?1, a core cytokine in airway remodeling, to explore whether lncRNAs are involved in the occurrence of chronic obstructive pulmonary disease (COPD). We identified a novel lncRNA ENST00000440406 which was highly associated with TGF-?1 and named it HSALR1 (HSP90AB1 associated lncRNA 1). Results showed that this lncRNA was an amplifier of the non-canonical pathway of TGF-? signaling in HBFs. Mechanistically, the TGF-?1/Smad3 signaling pathway positively regulated HSALR1. Moreover, HSALR1 could directly bind to HSP90AB1 to promote the stabilization between HSP90AB1 and p-Akt, thereby leading to continuous activation of the Akt signaling pathway. Meanwhile, mice carrying HSALR1 with adeno-associated virus (AAV-HSALR1) also confirmed that HSALR1 can promote the development of COPD. In conclusion, it was evident that the lncRNA could act as a scaffold of the protein complex to enhance continuous activation of downstream pathways, ultimately promoting cell proliferation.