Massaro Donald, Massaro Gloria Decarlo
Lung Biology Laboratory, Box 571481, Georgetown University School of Medicine, 3900 Reservoir Road, NW, Washington, DC 20057-1481, USA.
Proc Am Thorac Soc. 2006 Nov;3(8):709-12. doi: 10.1513/pats.200605-127SF.
In humans, age results in loss of pulmonary alveoli; menopause accelerates loss of diffusing capacity, an index of alveolar surface area; and disease (e.g., chronic obstructive pulmonary disease) results in loss of alveoli. Thus, an important goal for investigators is to generate knowledge that allows induction of pulmonary alveolar regeneration in humans. Our enthusiasm for this goal and our assessment of its feasibility are based on work in several laboratories over the last decade that has disproved the notion that pulmonary alveoli are incapable of regeneration, and on the growing evidence that signals that regulate programs of alveolar turnover (loss and regeneration) are conserved from rodents to humans. We review animal models of alveolar loss and regeneration and their conservation during evolution, and hence their relevance to humans.
在人类中，年龄增长会导致肺泡数量减少；绝经会加速弥散能力（肺泡表面积的一个指标）的丧失；而疾病（如慢性阻塞性肺疾病）会导致肺泡丧失。因此，研究人员的一个重要目标是获取知识，从而能够在人类中诱导肺泡再生。我们对这一目标的热情以及对其可行性的评估，是基于过去十年多个实验室的研究工作，这些工作推翻了肺泡无法再生的观点，同时也基于越来越多的证据表明，从啮齿动物到人类，调节肺泡更新（丧失和再生）程序的信号是保守的。我们综述了肺泡丧失和再生的动物模型及其在进化过程中的保守性，以及它们与人类的相关性。
