SPATA22 heterozygous variants drive premature ovarian insufficiency: mechanism of granulosa cells dysfunction and therapeutic potential of N-acetylcysteine (NAC) treatment
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This study investigates the role of SPATA22 heterozygous variants in driving premature ovarian insufficiency (POI) and explores the underlying mechanisms of granulosa cell dysfunction. The authors identify SPATA22 as a causative gene for POI, demonstrating that its defects lead to granulosa cell dysfunction and impaired fertility, while also showing that N-acetylcysteine (NAC) treatment can mitigate these effects and restore some ovarian function.
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