Metabolic, epigenetic, and immune crosstalk in ovarian aging

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Ovarian aging, marked by follicle depletion and oocyte quality decline, involves complex metabolic alterations. This review synthesizes evidence that dysregulated metabolic reprogramming, encompassing energy, lipid, and nutrient metabolism, drives ovarian functional decline. Central to this process is a self-reinforcing "metabolism-epigenetics-immunity" triangular network, where mitochondrial dysfunction and NAD + depletion disrupt epigenetic regulation and activate chronic inflammation, collectively accelerating follicular atresia and hormonal dysfunction. By integrating this mechanistic framework, we highlight emerging intervention strategies targeting metabolic hubs, such as mitochondrial rescue and senescent cell clearance, which offer new avenues for preserving ovarian function. This work provides a conceptual foundation for developing personalized strategies to mitigate reproductive aging and its systemic health impacts.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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