Engineering artificial ovaries: biology, scaffolds, and the clinical boundary of menopause reversal

Menopause is a time-locked consequence of a finite, embryonically
established ovarian reserve and network-level endocrine aging.
Here we synthesize mechanisms of primordial follicle dormancy
and activation (FOXO3–PI3K–AKT–AMH), evaluate current
cryopreservation limits, and propose engineered artificial ovary
concepts (endocrine-only vs. fertility-enabled). We argue artificial
ovaries can restore partial endocrine function but are unlikely to
reverse entrenched systemic aging; translational-priorities include
safe scaffolds, rapid vascularization, and stringent regulatory
oversight.