Fragile lungs or lung dysfunction can significantly impact a patient's quality of life. Currently, no specific treatment exists to prevent lung dysfunction in elderly patients. The detailed mechanism of fragile lungs or lung dysfunction in elderly patients remains elusive, and this study aimed to clarify it. General data and blood specimens were obtained from patients with fragile lungs or lung dysfunction. The mice were exposed to cigarette smoke using a smoking apparatus to induce fragile lungs or lung dysfunction mice model. Blood samples and lung tissues were collected from all groups for further testing. haematoxylin-eosin (HE) staining, immunofluorescence, Western blot, flow cytometry and quantitative reverse transcriptase PCR (qRT-PCR) were used to elucidate the molecular mechanisms of multidimensional integrated lung protection measures (MILPM) in fragile lungs or lung dysfunction mice by targeting the AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) pathway. The results indicated that upregulation of the AMPK/SIRT1 signalling pathway accelerates the fragile lungs or lung dysfunction process, whereas downregulation of the AMPK/SIRT1 signalling pathway can prevent it. Similarly, the change of forced vital capacity (FVC), total lung capacity (TLC) levels is associated with the fragile lungs or lung dysfunction process, whereas reducing their levels can serve as a preventative method against fragile lungs or lung dysfunction development. Upregulation of the AMPK/SIRT1 pathway can accelerate the process of fragile lungs or lung dysfunction.