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.
Keywords: AECII; COPD; CPFE; EMT; ER; FF; FIP; Hsp27; IPF; LAM5γ2; SASP; TGF; UIP; UPR; chronic obstructive pulmonary disease; combined pulmonary fibrosis and emphysema; endoplasmic reticulum; epithelial mesenchymal transition; familial interstitial pneumonia; fibroblast foci; heat shock protein 27; idiopathic pulmonary fibrosis; laminin-5-γ2 chain; senescence-associated secretory phenotype; transforming growth factor; type-II alveolar epithelial cells; unfolded protein response; usual interstitial pneumonia.
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