Ranatunga Sriyani, Pascoe Christopher D
Department of Physiology & Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada.
Biology of Breathing Theme, Children's Hospital Research Institute of Manitoba, Winnipeg, Manitoba, Canada.
Am J Physiol Lung Cell Mol Physiol. 2025 Jul 1;329(1):L126-L133. doi: 10.1152/ajplung.00046.2025. Epub 2025 Jun 4.
Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death worldwide, is traditionally considered a disease of smoking. However, <20% of people who smoke develop COPD, indicating the disease is complex, resulting from the interplay of genetic and environmental factors. Emerging evidence highlights the importance of exposure in early life to environmental irritants that impair fetal lung development and subsequent lung function trajectories, increasing risk for future COPD. Specifically, childhood asthma, preterm birth, and surfactant deficiency have been associated with lung function impairments and an increased COPD risk later in life. Furthermore, prenatal exposure to cigarettes influences sensitivity of individuals to smoking in their later life. A mounting body of evidence now indicates that diabetes exposure during pregnancy increases the risk for several childhood conditions linked to COPD risk, suggesting that maternal diabetes may be an unexplored risk factor for COPD. This article reviews the current literature on the influence of maternal diabetes on known early-life COPD risk factors (asthma and preterm birth), and identifies knowledge gaps that need to be addressed to pindown a potential association with COPD. Specifically, whether exposure to maternal diabetes influences offspring risk for COPD through already identified risk modifiers, or directly by altering lung function trajectories or sensitivity to cigarettes. Maternal diabetes rates are rising worldwide, with type 2 diabetes mellitus (T2DM) during pregnancy and gestational diabetes mellitus (GDM) nearly doubling over the last 15 years. Understanding how prenatal diabetes influences COPD risk is imperative to establishing whether intervening early can prevent COPD in this population.
慢性阻塞性肺疾病（COPD）是全球第四大死因，传统上被认为是一种与吸烟有关的疾病。然而，只有不到20%的吸烟者会患上COPD，这表明该疾病很复杂，是由遗传和环境因素相互作用导致的。新出现的证据凸显了早年接触损害胎儿肺发育及后续肺功能轨迹的环境刺激物的重要性，这会增加未来患COPD的风险。具体而言，儿童哮喘、早产和表面活性剂缺乏与肺功能损害及晚年患COPD风险增加有关。此外，产前接触香烟会影响个体在晚年对吸烟的敏感性。现在越来越多的证据表明，孕期接触糖尿病会增加与COPD风险相关的几种儿童疾病的风险，这表明母体糖尿病可能是一个尚未被探索的COPD风险因素。本文综述了关于母体糖尿病对已知的早年COPD风险因素（哮喘和早产）影响的现有文献，并确定了为确定与COPD的潜在关联而需要填补的知识空白。具体来说，接触母体糖尿病是否通过已确定的风险调节因素影响后代患COPD的风险，还是直接通过改变肺功能轨迹或对香烟的敏感性来影响。全球范围内母体糖尿病发病率正在上升，妊娠期间的2型糖尿病（T2DM）和妊娠期糖尿病（GDM）在过去15年中几乎翻了一番。了解产前糖尿病如何影响COPD风险对于确定早期干预是否可以预防该人群患COPD至关重要。
