Currently, diabetes has become the third type of non-communicable disease that endangers human health, and its chronic complications have become an important cause of disability and death in diabetic patients. The chronic complications of diabetes, such as diabetic cardiovascular disease, diabetic nephropathy, diabetic retinopathy, diabetic peripheral neuropathy, etc., have been widely recognized and studied, but little research has been done on the effects of diabetes on pulmonary lesions. With the continuous research on its chronic complications, the pulmonary changes caused by diabetes are being gradually recognized. In recent years, scholars at home and abroad have done a lot of research work on the changes in pulmonary function caused by diabetes, trying to understand the pulmonary pathological changes in diabetes and the possible mechanisms of pulmonary damage. As early as the 1970s, Schuyler et al. reported for the first time that young patients with type 1 diabetes who had no history of pulmonary disease, allergy or smoking had reduced pulmonary function tests (PFTs) such as diffusion of carbon monoxide (DLCO), pulmonary elastic retraction force, lung volume and maximal forceful respiration, which were thought to be caused by diabetes affecting pulmonary elastin, and were at risk of developing chronic airflow obstruction. Sandler et al. and Luo Mei et al. also found that reduced DLCO in type 1 diabetic patients was accompanied by reduced pulmonary capillary blood volume, because the ability of carbon monoxide (CO) transport was mainly affected by the integrity of pulmonary capillary endothelial cells. Since then, attention has been paid to the changes in pulmonary vascularity in diabetes, and a lot of research work has been done on the changes in pulmonary function in diabetes by scholars at home and abroad. The cause of pulmonary function impairment in diabetic patients is not clear, but autopsy materials from foreign scholars on diabetic and non-diabetic patients confirmed that the pulmonary artery wall, alveolar capillary basement membrane, alveolar epithelium and alveolar wall were significantly thicker in diabetic patients than in non-diabetic patients, which provided a pathological basis for diabetic lung involvement. After electron microscopic observation of lung tissue biopsy specimens from type 2 diabetic patients, it was found that there was diffuse thickening of the basal plate between the alveolar epithelium and capillary endothelium with onion skin-like changes, protein deposits around the basal plate and mixed with the basal plate, individual microvascular stenosis or even occlusion; irregular deposits of high electron density material were seen at the distal end of the microvessels; endothelial cells and pericytes within The pools of rough endoplasmic reticulum were dilated, large phagosomes (vesicles) were formed, and type II alveolar cells were rounded and small; cell surface villi disappeared, osmiophilic lamellar vesicles were significantly reduced and atrophied, and osmiophilic vesicles lost their lamellar structure and formed a high electron density solid mass; intracytoplasmic rough endoplasmic reticulum and mitochondria were cystically dilated, and there seemed to be translucent material inside the vesicles, indicating that lung tissue of early diabetic patients did have This suggests that microangiopathy and impaired synthesis and secretion of pulmonary surface active substances may be present in the lung tissue of early diabetic patients, leading to alveolar collapse and changes in lung function. In a study by Zhuo-jie et al, the basement membrane of alveolar capillary endothelial cells in diabetic rats was significantly thicker than that of normal controls under electron microscopy, and the thickening of the substrate increased the oxygen diffusion distance and affected the gas exchange function. It also affects the ventilation/blood flow ratio. It has been suggested that there are abnormalities in pulmonary capillaries and surface active substances when arterial partial pressure of oxygen (PaO2) is reduced in diabetic patients, and such abnormal changes may be an important cause of pulmonary dysfunction. Shen Xingping et al. reported that lung extracellular matrix abnormalities were already present in rats at 4 weeks of diabetes, with increased synthesis and decreased degradation of connective tissue proteins, as evidenced by increased and thickened elastic fibers and collagen fibers, and increased levels of type IV collagen and laminin distributed in cords and threads in alveolar septa, fine bronchial basement membranes, small vessels and capillary basement membranes. The non-enzymatic glycosylation of collagen during hyperglycemia reduces collagen degradation and causes collagen accumulation, while the formation of advanced glycosylation end products (AGES) acts on type IV collagen to reduce its elasticity and stiffen it. The thickening of the basement membrane and the basement membrane of the pulmonary vasculature decreased the diffusion function of the lung and ultimately led to a decrease in pulmonary ventilation and pulmonary diffusion function. Zhang Hong et al. used transmission electron microscopy to observe lung tissue biopsies from 10 patients with type 2 diabetes mellitus combined with lung cancer, and found that: the alveolar tissue of lung type II became smaller, the surface microvilli disappeared, the osmiophilic lamellar vesicles atrophied and lost their lamellar structure, forming a high electron density solid mass; the rough endoplasmic reticulum and mitochondria were cystically dilated, with translucent material deposited inside, reduced euchromatin and heterochromatin condensed; the alveolar epithelium and mitochondria were cystically dilated. The alveolar epithelium and interstitial basement membrane were diffusely thickened with onion skin-like changes, surrounded by protein deposits and fused with the basement membrane. This suggests that the lung is the target organ of the chronic “attack” of diabetes mellitus, and the histopathological changes of the lung caused by diabetes mellitus have their own characteristics different from those of other lung diseases, which are the pathological basis of the abnormal lung function.