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In studies of GPX5 knockout mice, we deduced that GPX5 is a way to maintain the integrity of sperm DNA function by removing excess H 2 O 2 , and these mice did not exhibit significant defects in the epididymis and sperm cells ( 2 O 2 scavengers was detected (Noblanc et al., 2012), proving that after SNGPX4 and GPX5 double knockouts, the epididymal tissues of mice produced oxidative stress responses, indicating that SNGPX4 and GPX5 play a role in maintaining the normal structure of the sperm nucleus in the epididymal tissue (Noblanc et al., 2012)
Although animal models present challenges in studying NPS, they offer invaluable insights into the potential underlying mechanisms
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Research reveals that platinum-resistant HGSOC cells often exhibit suppression of Homologous Recombination (HR) repair pathways, while alternative repair mechanisms, such as Non-Homologous End Joining (NHEJ), are activated ( Single-cell RNA sequencing has revealed specific drug-resistant cell subpopulations in HGSOC that promote their growth and drug resistance through interactions with fibroblasts and endothelial cells in the tumor microenvironment ( 3.3 Apoptosis and autophagy In the apoptotic pathways of tumor cells and HGSOC cells, key proteins such as the Bcl-2 family, p53, and caspases play crucial roles ( p53, as a tumor suppressor, promotes apoptosis by inducing the expression of apoptosis-related genes, particularly in cases of DNA damage ( Autophagy plays a dual role in the drug resistance of tumor cells and HGSOC
