https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41157 Wed 15 Feb 2023 10:57:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44253 Tue 11 Oct 2022 12:28:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44861 Thu 27 Oct 2022 13:56:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33903 Thu 24 Mar 2022 11:29:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39904 Thu 14 Jul 2022 11:58:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55279 Mon 13 May 2024 15:32:02 AEST ]]> https://nova.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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46080 Fri 11 Nov 2022 10:10:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36769 Fri 03 Jul 2020 14:34:42 AEST ]]>