Type 1 Diabetes Mellitus is an Independent Risk Factor for Pulmonary Fibrosis (Retracted article. See FEB, 2023)
Type 1 Diabetes Mellitus is an Independent Risk Factor for Pulmonary Fibrosis (Retracted article. See FEB, 2023)
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DOI：
10.1007/s12013-014-0068-4
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发表时间：
2014-11-01
影响因子：
2.6
通讯作者：
Yang, Junling
中科院分区：
文献类型：
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作者：
Hu, Yuxin;Ma, Zhongsen;Yang, Junling
本研究的目的是评估肺纤维化和1型糖尿病之间的临床和组织病理学关系。我们检查了12例出现呼吸困难的1型糖尿病患者的临床肺功能参数和经支气管肺活检，以评估相关的组织病理学变化。肺部CT图像肺功能测试12例糖尿病患者无呼吸困难和12名匹配的正常人作为对照。在诱导实验性糖尿病后，对小鼠的肺组织进行了类似的组织病理学分析，包括细胞因子水平和促纤维化标志物，试图加强糖尿病和肺纤维化之间的联系。与对照组相比，有呼吸困难和无呼吸困难的糖尿病患者的肺功能参数（FVC、FEV 1、TLC和DLco/VA）显著降低。与正常对照组相比，两组患者的肺部CT评分和症状也有所增加，但增加最多的是伴有呼吸困难的糖尿病患者。小鼠中诱导的慢性高血糖导致肺部组织病理学变化，这些变化与人类糖尿病受试者中发现的变化相似，包括由炎症细胞浸润的增生性间质和本质上的纤维化造成的肺泡压缩。两个炎症相关基因，TNF-α和派-1，以及两个纤维化相关基因，CTGF和纤连蛋白，在糖尿病小鼠肺中表现出增加的mRNA和蛋白表达。总之，肺纤维化和1型糖尿病之间存在显著的临床和组织病理学相关性。糖尿病在临床上与人类的肺纤维化和功能障碍相关，并且在实验模型中糖尿病诱导导致类似的肺纤维化。这些临床和非临床数据表明，糖尿病是肺纤维化的独立危险因素。
The objective of this study was to assess the clinical and histopathological relationship between pulmonary fibrosis and type 1 diabetes. We examined clinical pulmonary function parameters and transbronchial lung biopsies to assess associated histopathological changes in 12 type 1 diabetic patients presenting with dyspnea. Lung CT images pulmonary function tests from 12 diabetic patients without dyspnea and from 12 matched normal subjects served as controls. A similar histopathological analysis, including cytokine levels and pro-fibrotic markers, was performed on lung tissues in mice after the induction of experimental diabetes in an attempt to strengthen the link between diabetes and pulmonary fibrosis. Pulmonary function parameters (FVC, FEV1, TLC, and DLco/VA) were significantly reduced in diabetic patients with dyspnea and without dyspnea, compared to controls. Both patient groups also had increased lung CT scores and symptoms compared to normal controls, though the greatest increases were in the diabetic patients with dyspnea. Chronic hyperglycemia induced in mice led to histopathological changes in the lungs that were similar to those found in the human diabetic subjects and included alveoli compression by hyperplastic interstitium infiltrated with inflammatory cells and fibrotic in nature. Two inflammatory related genes, TNF-alpha and PAI-1, and two fibrosis-related genes, CTGF and fibronectin, demonstrated increased mRNA and protein expression in diabetic mouse lungs. In conclusion, there were significant clinical and histopathological correlations between pulmonary fibrosis and the presence of type 1 diabetes. Diabetes was clinically associated with pulmonary fibrosis and dysfunction in humans, and diabetes induction led to a similar pulmonary fibrosis in an experimental model. These clinical and non-clinical data suggest that diabetes is an independent risk factor for pulmonary fibrosis.