Evidence for KISS-1 nuclear translocation and PI3K/AKT signaling in the ultrastructurally and morphometrically analyzed human endometriosis

These findings suggest a mechanistic link between PI3K/AKT signaling and nuclear KiSS-1 translocation as an adaptive response to chronic hypoxia and inflammation in endometrial cells. This interaction may regulate survival, proliferation, and fibrotic remodeling processes characteristic of endometriosis. This integrated ultrastructural and molecular analysis provides novel insights into the pathophysiological role of nuclear KiSS-1 and its potential as a diagnostic and therapeutic target in endometriosis.