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. Author manuscript; available in PMC: 2021 Aug 11.
Published in final edited form as: Nat Aging. 2021 Feb 11;1(2):205–217. doi: 10.1038/s43587-021-00027-5

Figure 8: Airway delivery of SIRT3 cDNA resolves age-associated persistent lung fibrosis in mice.

Figure 8:

Aged mice subjected to bleomycin lung injury develop persistent, non-resolving lung fibrosis. This non-resolving phenotype of lung injury-fibrosis is associated with decreased lung levels of SIRT3 and persistence of apoptosis-resistant myofibroblasts. Gene delivery of SIRT3 cDNA via the airway restores capacity for fibrosis resolution, which is associated with FoxO3 activation/translocation to the nucleus. Our studies support a cell non-autonomous mechanism by which airway macrophages uptake the SIRT3 cDNA plasmid and produce pro-resolution factor(s) that are able to activate FoxO3a in myofibroblasts and mediate anti-senescent and pro-apoptotic effects in these reparative cells.