The ovary is a dynamic organ where mechanical forces profoundly regulate follicular development, oocyte maturation, and overall reproductive function. These forces, originating from the extracellular matrix (ECM), granulosa and theca cells, and ovarian stroma, influence cellular behavior through mechanotransduction, translating mechanical stimuli into biochemical responses. This review explores the intricate interplay between mechanical cues and ovarian biology, focusing on key mechanosensitive pathways such as Hippo signaling, the PI3K/AKT pathway, and cytoskeletal remodeling, which govern follicular dormancy, activation, and growth. Additionally, it examines how ovarian aging disrupts the mechanical microenvironment, with ECM stiffening and altered mechanotransduction contributing to a decline in ovarian reserve and reproductive potential. Emerging technologies, including 3D culture systems and organ-on-chip platforms, are highlighted for their ability to replicate the ovarian microenvironment and advance drug discovery and therapeutic interventions. By integrating mechanobiological principles, this review aims to enhance our understanding of ovarian function and provide new strategies for preserving fertility and combating infertility.

Ovarian aging is the process of decline in ovarian reserve, endocrine function with age, leading to reduced fertility and increased risk of various related diseases. In recent years, medicine food homology (MFH) species have attracted much attention for their potential to delay ovarian aging due to their dietary and medicinal values. In this review, we have focused on the intervention of MFH species and active ingredients on ovarian aging, with an emphasis on the molecular mechanisms involved in antioxidant, anti-inflammatory, apoptosis inhibitory, balance of autophagy, maintenance of genome stability, mitochondrial function protective and estrogen-like effects through multiple signaling pathways (e.g., PI3K/Akt, Nrf2/HO-1, SIRT1/mTOR, Nrf2/ARE, etc.). Possessing the characteristics of multi-pathway and multi-target effects, MFH species and active ingredients provide new ideas for the research and development of health food and functional preparations. High-quality clinical studies are still needed for verification.

Micro- and nanoplastics (MNPs) are widely distributed and persistent in the environment. They can enter the body through ingestion, inhalation, and dermal contact, and their potential effects on female reproductive health have drawn increasing attention. Oocytes are central to female reproductive function. However, the mechanisms underlying MNP toxicity to oocytes, as well as their intergenerational and transgenerational effects, remain poorly understood. This review searched databases such as PubMed and Web of Science. By integrating evidence from diverse animal models and human samples, it summarizes the potential effects of MNPs on oocytes and the related molecular mechanisms. The findings indicate that MNPs may impair oocyte development via oxidative stress, inflammation, endoplasmic reticulum stress, endocrine disruption, and epigenetic modifications. These processes are associated with changes in the Wnt/β-catenin, NOD-like receptor family pyrin domain containing 3 (NLRP3)/caspase-1, Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB), and protein kinase R-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2 alpha (eIF2α) signaling pathways, and are linked to mitochondrial dysfunction, apoptosis, meiotic defects, chromosomal abnormalities, and impaired oocyte maturation. Animal studies further suggest that maternal exposure to MNPs may impair offspring development and reproductive function. However, evidence for true transgenerational effects remains limited. Notably, most existing evidence comes from animal studies, many of which used standardized polystyrene (PS) particles. Although MNPs have been detected in human biological samples, their actual effects on human reproductive health remain to be clarified. Graphical