
Senescent cells can drive age-related tissue dysfunction partially via a senescence-associated secretory phenotype (SASP) involving proinflammatory and profibrotic factors. Cellular senescence has been associated with a structural and functional decline during normal lung ageing and age-related diseases such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Lung tissues from elderly persons with asthma showed more significant airway fibrosis than age-matched elderly persons with nonasthma and young controls. In addition, lung tissue or isolated ASM cells from elderly persons with asthma showed increased expression of multiple senescent markers, including phospho-p53, p21, telomere-associated foci (TAF), and multiple SASP components. Senescence and SASP components were also increased with ageing per se. These data highlight the presence of cellular senescence in AIE that may contribute to airway remodelling.
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