Research Paper Volume 15, Issue 24 pp 15382—15401

Proteomic analysis reveals the aging-related pathways contribute to pulmonary fibrogenesis

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Figure 8. Assessment of circANKRD42 and cytoskeleton in the healthy population and the key molecular players in aging and pulmonary fibrosis. (A) qRT-PCR result showed that circANKRD42 expression increased with age in a healthy-population group. (B) Phalloidin staining depicted that the cytoskeleton became disorder and underwent disorganized expansion in aging humans compared with young ones. (C) Fluorescence images showed that F-actin increased in 60-year-old healthy people compared with that in 11-year-old ones. (D) Key molecular players were involved in aging and pulmonary fibrosis, including epigenetic alteration (lncIAPF and circANKRD42), mitochondrial dysfunction, abnormal ferroptosis, autophagy, and mechanical forces.