Hepatic KLF9 Deficiency Inhibits Dehydroepiandrosterone (DHEA)-Induced Polycystic Ovary Syndrome via Liver-Ovary Axis.

ABSTRACT: Hyperandrogenism is one of the key leading causes of polycystic ovary syndrome (PCOS), which is a complex metabolic disorder affecting 6% to 20% of women of reproductive age. However, the molecular pathogenetic mechanisms responsible for androgen excess in PCOS remain largely unknow. While most previous studies have specifically focused on ovarian tissue, few have evaluated the role of extraovarian organs in PCOS. Here, it is found that KLF9 expression is up-regulated in murine primary hepatocytes treated with DHEA. Notably, the genetic ablation of Klf9 in hepatocytes significantly alleviated the progression of DHEA induced PCOS in mouse. Conversely, hepatic Klf9 transgenic mice displayed a spontaneous PCOS-like phenotype. Mechanistically, hepatic KLF9 is directly activated by intranuclear

SUBMITTER: Song J 

PROVIDER: S-EPMC12752638 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature