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presented a heterozygous CHAC1 deletion mouse model that was protected from kidney disease progression across three different disease models, without any known phenotypic changes under control conditions ( Despite its injury-promoting effects in some organs, CHAC1 contributes to tissue repair in certain contexts

Intracellular GSH levels and the expression of antioxidant enzymes (NRF2, GPX4 and SOD1) were evaluated in tumor tissues in 51 patients receiving neoadjuvant chemotherapy