Polycystic ovary syndrome (PCOS) is the most common reproductive endocrine disorder affecting women, which can lead to infertility. Infertility, obesity, hirsutism, acne, and irregular menstruation are just a few of the issues that PCOS can be linked to. PCOS has a complicated pathophysiology and a range of clinical symptoms. Chronic low-grade inflammation is one of the features of PCOS. The inflammatory environment involves immune and metabolic disturbances. Numerous organ systems across the body, in addition to the female reproductive system, have been affected by the pathogenic role of immunological dysregulation in PCOS in recent years. Insulin resistance and hyperandrogenism are associated with immune cell dysfunction and cytokine imbalance. More importantly, obesity is also involved in immune dysfunction in PCOS, leading to an inflammatory environment in women with PCOS. Hormone, obesity, and metabolic interactions contribute to the pathogenesis of PCOS. Hormone imbalance may also contribute to the development of autoimmune diseases. The aim of this review is to summarize the pathophysiological role of immune dysregulation in various organ systems of PCOS patients and provide new ideas for systemic treatment of PCOS in the future.

In women who are getting older, the quantity and quality of their follicles or oocytes and decline. This is characterized by decreased ovarian reserve function (DOR), fewer remaining oocytes, and lower quality oocytes. As more women choose to delay childbirth, the decline in fertility associated with age has become a significant concern for modern women. The decline in oocyte quality is a key indicator of ovarian aging. Many studies suggest that age-related changes in oocyte energy metabolism may impact oocyte quality. Changes in oocyte energy metabolism affect adenosine 5'-triphosphate (ATP) production, but how related products and proteins influence oocyte quality remains largely unknown. This review focuses on oocyte metabolism in age-related ovarian aging and its potential impact on oocyte quality, as well as therapeutic strategies that may partially influence oocyte metabolism. This research aims to enhance our understanding of age-related changes in oocyte energy metabolism, and the identification of biomarkers and treatment methods.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with infertility and poor reproductive outcomes. The follicular fluid (FF) microenvironment plays a crucial role in oocyte development. This review summarizes evidence elucidating the alterations in FF composition in PCOS. Various studies demonstrated a pronounced proinflammatory milieu in PCOS FF, characterized by increased levels of cytokines, including but not limited to interleukin-6 (IL-6), tumor necrosis factor α, C-reactive protein, and IL-1β, concomitant with a reduction in anti-inflammatory IL-10. T lymphocytes and antigen-presenting cells are dysregulated in PCOS FF. PCOS FF exhibit heightened reactive oxygen species production and the accumulation of lipid peroxidation byproducts, and impaired antioxidant defenses. Multiple microRNAs are dysregulated in PCOS FF, disrupting signaling critical to granulosa cell function. Proteomic analysis reveals changes in pathways related to immune responses, metabolic perturbations, angiogenesis, and hormone regulation. Metabolomics identify disturbances in glucose metabolism, amino acids, lipid profiles, and steroid levels with PCOS FF. Collectively, these pathological alterations may adversely affect oocyte quality, embryo development, and fertility outcomes. Further research on larger cohorts is needed to validate these findings and to forge the development of prognostic biomarkers of oocyte developmental competence within FF. Characterizing the follicular environment in PCOS is key to elucidating the mechanisms underlying subfertility in this challenging disorder.

Background: Sarcopenia and frailty are both age‐related declines in functional reserve that are linked to adverse health outcomes. It is critical to know about the outcomes of a combination of these conditions. The study aimed to investigate the effects of sarcopenia and frailty on postoperative recovery in elderly patients and to explore risk factors.Methods: This prospective cohort study was conducted among 608 patients aged ≥60 years, American Society of Anesthesiologists I‐III, who were scheduled to undergo thoracic (non‐cardiac) and abdominal surgery from 1 March 2022 to 31 October 2022 at the Affiliated Hospital of Xuzhou Medical University. Frailty was measured by the 28‐item frailty index, and sarcopenia was assessed sarcopenia was assessed by skeletal muscle index in computed tomographic scan, handgrip strength and 6‐m walk. Participants were classified as follows: Group A: both sarcopenia and frailty; Group B: sarcopenia only; Group C: frailty only; and Group D: neither frailty nor sarcopenia. The primary outcome was 90‐day morbidity. Multivariable logistic regression model was used to estimate the association between sarcopenia, frailty and 90‐day morbidity.Results: The median (interquartile range) age of participants was 68 (64–72) years, and 62.7% were men. The prevalence rates of sarcopenia and frailty were 32.8% and 47.6%, respectively. The 90‐day morbidity in Group A was 58.5%, in Group B was 46.2%, in Group C was 42.0% and in Group D was 28.8%, and the difference was significant (P < 0.001). In the multivariable analysis, both sarcopenia and frailty [odds ratio (OR), 2.21; 95% confidence interval (CI), 1.26–3.89], sarcopenia only (OR, 1.84; 95% CI, 1.01–3.36), frailty only (OR, 1.77; 95% CI, 1.03–3.03), women (OR, 0.67; 95% CI, 0.45–0.99), body mass index (OR, 0.94; 95% CI, 0.88–0.99), pre‐operative albumin (OR, 0.96; 95% CI, 0.91–1.00) and operative stress score (OSS) [OSS 3 (OR, 2.09; 95% CI, 1.21–3.67); OSS 4–5 (OR, 3.81; 95% CI, 2.31–6.42)] were independently associated with 90‐day morbidity. In the multivariable analysis with inverse probability weighting adjusted cohort, sarcopenia and frailty were also significantly associated with 90‐day morbidity.Conclusions: Sarcopenia and frailty were associated with higher risks of postoperative 90‐day morbidity in elderly patients alone and in combination. Sex, body mass index, pre‐operative albumin and operative stress were also independent factors for postoperative morbidity within 90 days.

Successful pregnancy requires the maternal immune system to tolerate the semi-allogeneic embryo. A good trophoblast function is also essential for successful embryo implantation and subsequent placental development. Chemokines are initially described in recruiting leukocytes. There are rich chemokines and chemokine receptor system at the maternal–fetal interface. Numerous studies have reported that they not only regulate trophoblast biological behaviors but also participate in the decidual immune response. At the same time, the chemokine system builds an important communication network between fetally derived trophoblast cells and maternally derived decidual cells. However, abnormal functions of chemokines or chemokine receptors are involved in a series of pregnancy complications. As growing evidence points to the roles of chemokines in pregnancy, there is a great need to summarize the available data on this topic. This review aimed to describe the recent research progress on the regulation and function of the main chemokines in pregnancy at the maternal–fetal interface. In addition, we also discussed the potential relationship between chemokines and pregnancy complications.

Polycystic ovary syndrome (PCOS) is a complex common endocrine disorder affecting women of reproductive age. Ovulatory dysfunction is recognized as a primary infertile factor, however, even when ovulation is medically induced and restored, PCOS patients continue to experience reduced cumulative pregnancy rates and a higher spontaneous miscarriage rate. Hyperandrogenism, a hallmark feature of PCOS, affects ovarian folliculogenesis, endometrial receptivity, and the establishment and maintenance of pregnancy. Decidualization denotes the transformation that the stromal compart of the endometrium must undergo to accommodate pregnancy, driven by the rising progesterone levels and local cAMP production. However, studies on the impact of hyperandrogenism on decidualization are limited. In this study, we observed that primary endometrial stromal cells from women with PCOS exhibit abnormal responses to progesterone during in vitro decidualization. A high concentration of testosterone inhibits human endometrial stromal cells (HESCs) decidualization. RNA-Seq analysis demonstrated that pyruvate dehydrogenase kinase 4 (PDK4) expression was significantly lower in the endometrium of PCOS patients with hyperandrogenism compared to those without hyperandrogenism. We also characterized that the expression of PDK4 is elevated in the endometrium stroma at the mid-secretory phase. Artificial decidualization could enhance PDK4 expression, while downregulation of PDK4 leads to abnormal decidualization both in vivo and in vitro. Mechanistically, testosterone excess inhibits IGFBP1 and PRL expression, followed by phosphorylating of AMPK that stimulates PDK4 expression. Based on co-immunoprecipitation analysis, we observed an interaction between SIRT1 and PDK4, promoting glycolysis to facilitate decidualization. Restrain of AR activation resumes the AMPK/SIRT1/PDK4 pathway suppressed by testosterone excess, indicating that testosterone primarily acts on decidualization through AR stimulation. Androgen excess in the endometrium inhibits decidualization by disrupting the AMPK/SIRT1/PDK4 signaling pathway. These data demonstrate the critical roles of endometrial PDK4 in regulating decidualization and provide valuable information for understanding the underlying mechanism during decidualization.