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Next, we found that CXCL10 directly bound to IL18R1 to impair ovarian function through three pathways: inducing ovarian fibrosis through p-JNKp-JUN COL1A1, promoting primordial follicle overactivation through p-AKTp-FOXO3A, and increasing ovarian inflammation through p-P65 IFN

DNA hypomethylation and human diseases

doi: 10.1016/j.bbamcr.2010.10.014

Future research should further investigate the specific mechanisms by which immune cells contribute to DKD, as well as explore how modulating immune responses can improve patient prognosis