https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52464 Wed 28 Feb 2024 15:57:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45148 Wed 26 Oct 2022 19:13:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45701 Tue 28 Mar 2023 15:44:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47646 Tue 24 Jan 2023 14:51:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30970 Thu 24 Mar 2022 11:31:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34569 Thu 04 Nov 2021 10:38:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46097 P < 0.05, n = 5–8). The targeting of cGAS also attenuated etoposide-induced senescence in Ctrl-LFs (P < 0.05, n = 5–8). Levels of mitochondrial DNA (mDNA) detected by qPCR in the cytosol and medium of IPF-LFs or senescence-induced Ctrl-LFs were higher than Ctrl-LFs at baseline (P < 0.05, n = 5–7). The addition of DNAse I (100 U/ml) deaccelerated IPF-LF senescence (P < 0.05, n = 5), whereas ectopic mDNA or the induction of endogenous mDNA release augmented Ctrl-LF senescence in a cGAS-dependent manner (P < 0.05, n = 5). In conclusion, we provide evidence that cGAS reinforces lung fibroblast senescence involving damaged self DNA. The targeting of cGAS to supress senescent-like responses may have potential important therapeutic implications in the treatment of IPF.]]> Fri 11 Nov 2022 11:23:00 AEDT ]]>