TL;DR
Despite remarkable progress, no intervention currently reverses ovarian ageing or reliably improves age-related oocyte competence, and bridging this gap will require rigorous translational research and careful, evidence-based clinical integration.
Ovarian aging is recognized as one of the earliest and most consequential manifestations of the aging process in women, preceding by decades the decline observed in most other organ systems and directly conditioning both reproductive potential and long-term health outcomes. Although anti-Müllerian hormone, antral folli...
This narrative review examines the biological basis of PRP, its potential effects on the ovarian niche, and the current clinical evidence supporting its use in women with diminished ovarian reserve, poor ovarian response, premature ovarian insufficiency, and advanced reproductive age and explores the rationale for comb...
Understanding how endocrine dysregulation interacts with metabolic, genomic, and epigenetic alterations and changes in the follicular microenvironment may facilitate the identification of biomarkers and the development of targeted approaches to preserve oocyte quality during reproductive aging.
A trafficking hypothesis rather than a demonstrated mechanism is advanced: a transcriptomic profile compatible with premature luteinization may be superimposed on disordered stage-dependent surface presentation and motivates prospective evaluation of biomarkers for stratified LH supplementation in assisted reproductive...
Female fertility has long been explained through observation of the ovarian follicle: the number of residing follicles and the quality of the oocyte. This review argues that the tissue surrounding those follicles involved in regulating cyclical ovarian remodelling is an additional contributor to female subfertility. Ov...
This Mini Review reframes POI as a process of inflammatory ovarian remodeling, in which immune activation, macrophage polarization, mitochondrial stress, inflammasome signaling, and inflammatory regulated cell death interact to accelerate follicular injury and ovarian reserve decline.
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