The adenosine monophosphate (AMP)-activated protein kinase (AMPK) signalling pathway regulates cell metabolism, inflammation and the immune response. This signalling pathway is essential for maintaining reproductive homeostasis and influencing steroidogenesis, implantation, and embryonic development. The central sensor, AMPK, regulates cell function in response to metabolic stress. The dysregulation of AMPK signalling has been implicated in several female reproductive disorders, including polycystic ovary syndrome (PCOS), endometriosis, infertility, and reproductive ageing. This review provides an overview of the role of AMPK in reproductive function and disorders, as well as potential therapeutic targets to restore balance in this signalling pathway. It discusses AMPK signalling in folliculogenesis, oocyte maturation, pregnancy maintenance, pre-eclampsia (PE) pathogenesis, PCOS, preterm birth, endometriosis, dysmenorrhoea and other disorders related to female reproduction. A deeper understanding of AMPK signalling in these contexts could provide new insights for the development of therapeutic interventions for reproductive health.

Phytochemical contents of honey are presumed to be beneficial to the female reproductive system (FRS). However, the biological effects of honey supplementation (HS) in vivo on the FRS remain unclear. This review aims to investigate the current literature on the effects of HS on the FRS, particularly on the sex hormone profile and reproductive organs (uterus and vagina). A systematic literature search using Scopus, MEDLINE via Ovid and Cochrane Library databases was conducted. Records were screened and identified for preclinical and clinical studies addressing the effects of HS on the FRS. Data on populations, interventions, outcomes and methodological quality were extracted. Studies were synthesised using tables and written summaries. Of the 198 identified records, six fulfilled the inclusion criteria. All six records were used for data extraction: two experimental studies using rats as the model organism and four human clinical studies of honey on female reproductive health. HS elevated the progesterone levels, restrained body weight increase, prevented uterine and vaginal atrophies in ovariectomised rats, attenuated symptoms of candidiasis and improved oxidative status in patients. Current evidence shows that short-term HS following surgical or physiological menopause exerts an oestrogenic, antioxidant and anti-inflammatory effect on the FRS. However, insufficient long-term studies preclude any definitive conclusions.

Concerns have arisen about the impact of wireless technology on male fertility, particularly regarding the duration of 2.45 GHz Wi-Fi radiation exposure. This study examines the influence of various exposure durations on sperm parameters and testicular histopathology, focusing on malondialdehyde as an oxidative stress marker. Twenty-four Sprague Dawley rats were exposed for eight weeks, after which their sperm concentration, motility, and viability and testicular histopathology were assessed. Malondialdehyde levels were measured using an Enzyme-Linked Immunosorbent Assay. One-way ANOVAs with Tukey’s post hoc tests were conducted for the sperm concentration, motility, and viability; the seminiferous epithelium height; and malondialdehyde. The Kruskal–Wallis H test was used for the Johnsen Score and seminiferous tubule diameter. The results indicated that 4 h of exposure to 2.45 GHz radiation induced oxidative stress and adversely affected sperm parameters and the testicular ultrastructure. Gradual recovery was observed at 8 h, with further improvement at 24 h, suggesting the activation of cell repair mechanisms. This was supported by significant changes in testicular organ coefficients, indicating potential recovery. Our findings suggest that Wi-Fi exposure reduces sperm fertility potential, with the body showing limited capacity for complete recovery from the damage.

In brief: Numerous studies have examined the impact of 2.45 GHz Wi-Fi exposure on the testes, highlighting concerns about its potential effects on male fertility. This study extends the investigation beyond the testes to include the epididymis, seminal vesicle and coagulating gland, providing a more comprehensive understanding of how 2.45 GHz Wi-Fi influences the male reproductive system. Numerous studies have documented the effect of 2.45 GHz Wi-Fi exposure on the testes and sperm quality. Nevertheless, detailed histological alterations of other male reproductive organs are underexplored. Therefore, this study aimed to evaluate detailed histological alterations of the testes, epididymis, seminal vesicle, coagulating organ and sperm parameters following 2.45 GHz Wi-Fi exposure. Eighteen adult male Sprague Dawley rats ( n = 18) were equally divided into three groups ( n = 6): control, 4 h and 24 h groups. The groups were exposed to an active router daily for 4 or 24 h, respectively. The control group was sham-exposed using an inactive router. The exposure lasted for 8 weeks at a 20 cm distance, with a power density of 0.141 W/m ² and a specific absorption rate of 0.41 W/Kg. Histological findings revealed vacuolation in the testes and the corpus epididymis of the 4 and 24 h groups. The seminal vesicle in both exposed groups exhibited multifocal atypical hyperplasia. Besides, the seminiferous tubule diameter decreased gradually in both exposed groups, with a substantial decrease in the 24 h group. The spermatogenesis index in 4 and 24 h groups also reduced significantly. The latter result was reflected in the sperm concentration, where both groups showed a significant reduction compared to the control group. Sperm motility also decreased significantly in the 4 h groups. Interestingly, there was a substantial increase in sperm viability in the 24 h group. These findings indicate that 2.45 GHz Wi-Fi exposure causes changes in the histology and histomorphometry measurement and impairs important sperm parameters. This highlights the consequences following Wi-Fi exposure on male reproductive health.

Pre-eclampsia, which is part of the spectrum of hypertensive pregnancy disorders, poses a significant health burden, contributing to maternal and infant morbidity and mortality. Pre-eclampsia is widely associated with persistent adverse effects on the cardiovascular health of women with a history of pre-eclampsia. Additionally, there is increasing evidence demonstrating that offspring of pre-eclamptic pregnancies have altered cardiac structure and function, as well as different vascular physiology due to the decrease in endothelial function. Therefore, early detection of the likelihood of developing pre-eclampsia-associated cardiovascular diseases is vital, as this could facilitate the undertaking of the necessary clinical measures to avoid disease progression. The utilisation of microRNAs as biomarkers is currently on the rise as microRNAs have been found to play important roles in regulating various physiological and pathophysiological processes. In regard to pre-eclampsia, recent studies have shown that the expression of microRNAs is altered in postpartum women and their offspring who have been exposed to pre-eclampsia, and that these alterations may persist for several years. This review, therefore, addresses changes in microRNA expression found in postpartum women and offspring exposed to pre-eclampsia, their involvement in cardiovascular disease, and the potential role of microRNAs to be used as predictive tools and therapeutic targets in future cardiovascular disease research.

Background/Objectives: The rapid rollout of 5G has renewed interest in potential reproductive effects of mid-band (3.5 GHz) and millimeter-wave (24 GHz) radiofrequency electromagnetic fields (RF-EMF). We examined frequency- and duration-dependent changes in testicular cytokines, apoptosis-related genes, and sperm quality in rats. Methods: Male Sprague Dawley rats (n = 6 per group) were exposed for 60 days to 3.5 GHz or 24 GHz RF-EMF for 1 h/day or 7 h/day. The sham controls were housed identically. Testicular expressions of IL-10, IL-6, IL-1β, and TNF-α were quantified; Tp53, Bax, Bcl2, and Casp3 mRNA expressions were measured; and sperm concentration, viability, and motility were evaluated. Results: IL-10 was significantly reduced in the 24 GHz group at both 1-h and 7-h exposure duration. At 7 h, TNF-α was also lower at 24 GHz. Casp3 expression was higher and Tp53 was lower at 3.5 GHz at 1-h exposure duration. Sperm concentration and viability were reduced after 24 GHz exposure at 7 h, while sperm motility was reduced after 3.5 GHz exposure at both durations. Conclusions: Exposure to RF-EMF 3.5 GHz primarily impacts sperm motility via extrinsic pro-apoptotic pathways, while exposure to 24 GHz impacts sperm concentration and viability potentially through immune–apoptotic mechanisms, with all negative effects amplified by 7-h daily exposure.