RESUMEN
Uterine fibroids (UFs) remain a significant health issue for many women, with a disproportionate impact on women of color, likely due to both genetic and environmental factors. The prevalence of UFs is estimated to be approximately 70% depending on population. UF-derived clinical symptoms include pelvic pain, excessive uterine bleeding, gastrointestinal and voiding problems, as well as impaired fertility. Nowadays numerous methods of UF treatment are available-from conservative treatment to invasive surgeries. Selecting an appropriate treatment option should be individualized and adjusted to the patient's expectations as much as possible. So far, the mainstay of treatment is surgery, but their negative impact of future fertility is clear. On the other hand, emerging new pharmaceutical options have significant adverse effects like liver function impairment, hot flashes, bone density loss, endometrial changes, and inability to attempt conception during treatment. Several natural compounds are found to help treat UFs and relieve their symptoms. In this review we summarize all the current available data about natural compounds that may be beneficial for patients with UFs, especially those who want to preserve their future fertility or have treatment while actively pursuing conception. Vitamin D, epigallocatechin gallate, berberine, curcumin, and others are being used as alternative UF treatments. Moreover, we propose the concept of using combined therapies of natural compounds on their own or combined with hormonal agents to manage UFs. There is a strong need for more human clinical trials involving these compounds before promoting widespread usage.
RESUMEN
The traditional view of follicle-stimulating hormone (FSH) as a reproductive hormone is changing. It has been shown that FSH receptors (FSHRs) are expressed in various extra-gonadal tissues and mediate the biological effects of FSH at those sites. Molecular, animal, epidemiologic, and clinical data suggest that elevated serum FSH may play a significant role in the evolution of bone loss and obesity, as well as contributing to cardiovascular and cancer risk. This review summarizes recent data on FSH action beyond reproduction.
RESUMEN
Premature ovarian insufficiency (POI) is a highly prevalent disorder, characterized by the development of menopause before the age of 40. Most cases are idiopathic; however, in some women the cause of this condition (e.g.; anticancer treatment, genetic disorders, and enzymatic defects) could be identified. Although hormone-replacement therapy, the principal therapeutic approach for POI, helps alleviate the related symptoms, this does not effectively solve the issue of fertility. Assisted reproductive techniques also lack efficacy in these women. Thus, an effective approach to manage patients with POI is highly warranted. Several mechanisms associated with POI have been identified, including the lack of function of the follicle-stimulating hormone (FSH) receptor, alterations in apoptosis control, mutations in Sal-like 4 genes, and thymulin or basonuclin-1 deficiency. The above mentioned may be good targets for gene therapy in order to correct defects leading to POI. The goal of this review is to summarize current experiences on POI studies that employed gene therapy, and to discuss possible future directions in this field.
RESUMEN
BACKGROUND: Previously, we reported a significantly higher prevalence of uterine fibroids (UFs) in African American women. This minority group also commonly suffers from vitamin D deficiency. We have demonstrated that 1,25(OH)2D3 attains a fibroid growth inhibitory impact through its ability to block the G1/S (gap 1/synthesis) phase of the cell cycle. Vitamin D is involved in DNA damage as well as in immune response regulation, anti-inflammation, autoimmunity and cancer. Since most of the prior data on vitamin D and UF were generated in vitro via established cell lines, it was necessary to verify and validate this observation in vivo using a diet-induced vitamin D-deficient mouse model. MATERIALS AND METHODS: Our model of vitamin D lacking function was established using 8-week exposure of C57/BL6 mice to vitamin D-deficient diet provides evidence of different functions accomplished by vitamin D in the regulation of myometrium homeostasis disrupted in the context of uterine fibroid. RESULTS: We found that vitamin D deficiency was associated with increased expression of sex steroid receptors in murine myometrium, increased expression of proliferation related genes, the promotion of fibrosis and enhanced inflammation, and promoted immunosuppression through Tregs expansion in murine myometrium. We also showed that a vitamin D deficient diet enhanced DNA damage in murine myometrium. CONCLUSION: Our model mimics the effects in humans that a lack of vitamin D has and propels the study of in vivo interaction between inflammation, genomic instability and cell proliferation in the myometrium.