In accordance with our findings, prior studies have illustrated that miR-135a-5p is druggable with schisandrin B to block the activation of NLRP3 inflammasome, consequently mitigating airway inflammation [51]; and miR-135a is also capable of repressing inflammation signaling pathways, α-SMA expression, and augmented E-cadherin expression to ultimately relieve pulmonary fibrosis [52]. Here, ACTA1 is linked to pulmonary fibrosis.