As a multifaceted adipokine, chemerin has been found to perform functions vital for immunity, adiposity, and metabolism through its three known receptors (chemokine-like receptor 1, CMKLR1; G-protein-coupled receptor 1, GPR1; C-C motif chemokine receptor-like 2, CCRL2). Chemerin and the cognate receptors are also expressed in the hypothalamus, pituitary gland, testis, ovary, and placenta. Accumulating studies suggest that chemerin participates in normal reproduction and underlies the pathological mechanisms of certain reproductive system diseases, including polycystic ovary syndrome (PCOS), preeclampsia, and breast cancer. Herein, we present a comprehensive review of the roles of the chemerin system in multiple reproductive processes and human reproductive diseases, with a brief discussion and perspectives on future clinical applications.

Meiosis is essential for sexual reproduction, yet the impact of microgravity on oocyte maturation remains unclear, raising concerns for reproductive success in space environments. Here, it is examined the effects of simulated microgravity (SMG) on mouse oocytes and found that SMG impaired mitochondrial function, evidenced by elevated oxidative phosphorylation and mitochondrial membrane hyperpolarization, resulting in meiotic arrest. This response is distinct from that induced by other stressors or seen in somatic cells under microgravity, highlighting the unique sensitivity of oocytes. SMG also caused mitochondrial mislocalization, which activated the unfolded protein response and suppressed mitochondrial gene expression. Despite accelerating meiotic progression, SMG delayed microtubule‐organizing center (MTOC) coalescence. This misalignment led to spindle defects, reduced polar body extrusion, and increased aneuploidy, compromising oocyte quality. The spindle assembly checkpoint (SAC) remained functional, suggesting mitochondrial dysregulation‐not SAC failure‐drives meiotic acceleration. Notably, even oocytes that reached maturation under SMG exhibited polarity loss and reduced developmental potential. Extending metaphase I by inhibiting the anaphase‐promoting complex rescued MTOC assembly and spindle formation, significantly improving maturation rates. These findings identify mitochondrial dysfunction as a key mediator of SMG‐induced meiotic failure and propose M‐phase regulation as a strategy to safeguard female fertility in space environments.

Ovarian endometriosis (OEM) is a chronic inflammatory condition that impairs ovarian function. While its effects on ovarian reserve are well established, the long-term consequences of OEM on ovarian dysfunction, premature ovarian failure (POF), and systemic health, particularly in the context of accelerated aging, remain insufficiently studied. In this study, we employed an OEM mouse model and bulk RNA sequencing to investigate the underlying mechanisms. Our results show that OEM accelerates primordial follicle depletion and upregulates mTOR signaling pathway gene expression, along with mechanical stress and paracrine signaling via the Hippo and Myc pathways. OEM also induces irregular estrus and ovarian fibrosis in aging mice, decreases serum AMH levels, and increases FSH levels. Systemically, elevated serum IgG levels contribute to osteoporosis and cognitive decline, both linked to ovarian dysfunction and POF in OEM. These findings elucidate the mechanisms driving premature ovarian reserve depletion in OEM and highlight its broader systemic effects. This study emphasizes the importance of monitoring ovarian health and ectopic tissue to safeguard ovarian reserves and mitigate long-term risks such as osteoporosis and cognitive decline.