Article
AARS2 R199C mutation induces lactylation-driven premature ovarian insufficiency phenotypes partially reversible by SIRT3.
Reproduction (Cambridge, England) - 5 Apr 2026
Zhang Hai-Hui, Zhang Zhi-Ling, Xu Wei
Abstract excerpt
In a homozygous alanine-tRNA synthetase 2 R194C knock-in mouse model (mimicking the human R199C -pathogenic variant), this study demonstrates that a single mutation can cause ovarian insufficiency in vivo and identifies the lactylation-metabolism-mechanistic target of rapamycin axis as the molecular driver of follicle exhaustion. Abstract Premature ovarian insufficiency (POI) often arises from genetic causes, yet...
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