
Aging Cell, Journal Year: 2024, Volume and Issue: unknown
Published: Nov. 4, 2024
Abstract Age‐related declines in oocyte quality and ovarian function are pivotal contributors to female subfertility clinical settings. Yet, the mechanisms driving aging senescence remain inadequately understood. The present study evaluated alterations N‐glycoproteins associated with noted a pronounced elevation N221 glycopeptides of cathepsin L (Ctsl) ovaries reproductive‐aged mice (8–9 months 11–12 months) compared younger counterparts (6–8 weeks). Subsequent analysis examined involvement Ctsl demonstrated significant levels aged oocytes. Further, it was revealed that overexpression young oocytes substantially diminished their quality, while expressing an N221‐glycosylation mutant did not suffer similar degradation. This finding implies glycosylation is modulating its effect on health. introduction inhibitor into culture medium restored by enhancing mitochondrial function, reducing accumulated reactive oxygen species (ROS), lowering apoptosis, recovering lysosome capacity. Furthermore, targeted downregulation using siRNA microinjection enhanced fertilization capability blastocyst formation, affirming role knockdown fostering embryonic developmental potential. In conclusion, these findings underscore detrimental effects high expression N‐glycosylated contribution senescence, highlighting as potential therapeutic target delay enhance viability.
Language: Английский