Key aging pathways including PI3K/AKT/mTOR, AMPK, and sirtuins drive ovarian decline through telomere attrition, mitochondrial dysfunction, and impaired autophagy. Targeted compounds like rapamycin (mTOR inhibitor), metformin (AMPK activator), resveratrol, and melatonin demonstrate mechanistic promise in preserving follicular reserves and oocyte quality. This convergence on fundamental longevity pathways represents a paradigm shift from symptom management to mechanistic intervention in reproductive aging. The implications extend far beyond fertility preservation. Since ovarian function governs systemic hormone production affecting bone density, cardiovascular health, and cognitive function, delaying ovarian aging could substantially impact women's healthspan. The approach mirrors successful longevity interventions in model organisms, suggesting reproductive aging may be more malleable than previously assumed. However, translating preclinical promise to clinical practice requires careful consideration of timing, dosing, and long-term safety profiles. The mechanistic overlap between ovarian aging and general aging processes positions reproductive health as a potential biomarker and intervention target for broader longevity strategies in women.