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. 2023 May 15;22(7):e13865. doi: 10.1111/acel.13865

FIGURE 6.

FIGURE 6

PINK1 deficiency activates cGAS‐STING pathway in aging mice model and tubular epithelial cells treated with H2O2. (a) The mRNA levels of cGAS and STING in Pink1+/+ and Pink1−/− mice kidney tissue at 4 and 24 months. (b) Western blotting of cGAS and STING in Pink1+/+ and Pink1−/− mice kidney tissue at 4 and 24 months. (c) The change of cGAS, STING, senescence signaling mediator and SASPs in siPINK1 and H2O2 treated cells on STING inhibitor, H‐151. (d) Schematic diagram summarizing role of PINK1 on renal aging. PINK1 deficiency enhances mitochondrial dysfunction known to be one of the STING activators, and eventually leads to renal aging presented by increased inflammatory response. Mean ± standard error of mean. (a) *p < 0.05, **p < 0.01, ***p < 0.001 vs. Pink1+/+ 4 M, # p < 0.05, ## p < 0.01, ### p < 0.001 vs. Pink1−/− 4 M, † p < 0.05, †† p < 0.01, ††† p < 0.001 vs. Pink1+/+ 24 M, M, months (c) *p < 0.05, **p < 0.01, ***p < 0.001 vs. siCONT+H2O2, # p < 0.05, ## p < 0.01, ### p < 0.001 vs. siPINK1+ H2O2, CONT, control.