Fig. 12

The aging lung with focus on ECM remodeling, immune response, senescence and pulmonary surfactant. The scheme highlights the complex interplay of ECM remodeling in healthy but aged lung and its link to immune response, senescence and surfactant lipids. The genomic landscape of the aging lung revealed extensive ECM remodeling which provided a rationale for an increased stiffness of the lung and damage of the basal membrane therefore contributing to an age-related emphysema. Additionally, we noticed an increased expression of genes coding for the senescence-associated secretory phenotype (SASP), thus augmenting inflammaging as well as immunosenescence. Finally, the genomic data of the aging lung indicated major changes in the production of pulmonary surfactant