PGE2-mediated aging microenvironment fuels pathogenic fibrosis in cesarean section scar defect

ABSTRACT: With the increasing rates of cesarean section (CS), cesarean section scar defect (CSD) has become an escalating clinical concern due to uterine dysfunction and reduced fertility. However, the biological basis of CSD remains poorly understood, particularly the mechanisms of impaired uterine repair and the causes of failure in conventional repair surgeries. This study integrates metabolomics, transcriptomics, a newly developed mouse model, and functional assays to elucidate the complex interplay between senescence and fibrosis in CSD. Our findings identify upregulation of PGES/PGE2 axis as a key upstream event that disrupts uterine healing. Elevated PGE2 preferentially induces early senescence of macrophages, which transmit pro-senescent signals to uterine fibroblasts through IL-1β/IL-1R sig

SUBMITTER: Yujia Yin 

PROVIDER: S-SCDT-10_1038-S44321-026-00521-6 | biostudies-other |

REPOSITORIES: biostudies-other