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Abstract：
Different anatomic and physiological changes occur in the lung of aging people that can affect pulmonary functions, and different pulmonary diseases, including deadly diseases such as chronic obstructive pulmonary disease (COPD)/emphysema and idiopathic pulmonary fibrosis (IPF), can be related to an acceleration of the aging process. The individual genetic background, as well as exposure to a variety of toxic substances (cigarette smoke in primis) can contribute significantly to accelerating pulmonary senescence. Premature aging can impair lung function by different ways: by interfering specifically with tissue repair mechanisms after damage, thus perturbing the correct crosstalk between mesenchymal and epithelial components; by inducing systemic and/or local alteration of the immune system, thus impairing the complex mechanisms of lung defense against infections; and by stimulating a local and/or systemic inflammatory condition (inflammaging). According to recently proposed pathogenic models in COPD and IPF, premature cellular senescence likely affects distinct progenitors cells (mesenchymal stem cells in COPD, alveolar epithelial precursors in IPF), leading to stem cell exhaustion. In this review, the large amount of data supporting this pathogenic view are discussed, with emphasis on the possible molecular and cellular mechanisms leading to the severe parenchymal remodeling that characterizes, in different ways, these deadly diseases.
摘要：
老年人的肺发生不同的解剖和生理变化，可以影响肺功能，和不同的肺部疾病，包括慢性阻塞性肺疾病（COPD）/肺气肿和特发性肺纤维化（IPF）等致命疾病，可能与老化过程的加速有关。个体的遗传背景,以及暴露于各种有毒物质（primis中的香烟烟雾）可以显着加速肺衰老。过早衰老可以通过不同的方式损害肺功能：通过特异性干扰损伤后的组织修复机制，从而扰乱间充质和上皮成分之间的正确串扰；通过诱导免疫系统的全身和/或局部改变，从而损害肺防御感染的复杂机制;并通过刺激局部和/或全身性炎症（炎症）。根据最近提出的COPD和IPF的致病模型，过早的细胞衰老可能影响不同的祖细胞(COPD中的间充质干细胞，IPF中的肺泡上皮前体)，导致干细胞耗尽.在这次审查中,讨论了支持这种致病观点的大量数据，强调可能的分子和细胞机制，导致严重的实质重塑的特征，以不同的方式，这些致命的疾病。
