Glutaminolysis regulates endometrial fibrosis in intrauterine adhesion via modulating mitochondrial function

Abstract

Glutaminolysis and glutaminolysis-associated mTOR signaling play a role in the activation of ESCs and the pathogenesis of endometrial fibrosis through regulating mitochondrial function. Glutaminolysis inhibition suppresses the activation of ESCs, which might be a novel therapeutic strategy for IUA.